Gastro exam 2

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Gastro exam 2
2013-11-14 18:49:56
gastro exam

gastro exam 2
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  1. What are the two disorders that make up inflammatory bowel disease?
    • ulcerative colitis
    • crohn's disease
  2. Chronic, recurrent disease characterized by diffuse mucosal inflammation involving only
    the colon, resulting in diffuse friability and erosions with bleeding; invariably involves the rectum, may extend proximally in continuous fashion to involve part or all of the colon.
    ulcerative colitis
  3. Chronic, recurrent disease characterized by patchy transmural inflammation involving any
    segment of the gastrointestinal tract from the mouth to the anus.
    crohn's disease
  4. What is the bimodal incidence of IBD? At what age are most patients diagnosed?
    • First peak occurs in 2nd and 3rd decades, second increase between 5th and 7th decades
    • Mean age for crohn's disease dx in N America is 15-30 yrs
    • Mean age for ulcerative colitis dx in N Amercia is 15-25 yrs
  5. What is the most common area in the small bowel affected by crohn's disease?
    terminal ileum (1/3 of cases)
  6. What are the considerations for crohn's disease as far as the percentage of cases involving different areas of the GI tract?
    • 50% involve small bowel and colon, most often the terminal ileum and adjacent proximal ascending colon (ileocolitis)
    • 30% involve only the small bowel, mostly terminal ileum (ileitis)
    • 20% involve the colon alone
  7. What are the major sites of involvement for crohn's disease?
    • terminal ileum
    • colon
    • ileocolon
    • upper GI tract
  8. Crohn's disease is a TRANSMURAL process that can result in what complications?
    • mucosal inflammation and ulceration
    • stricture
    • fistulous development
    • abscess formation
  9. What is strongly associated with the development of crohn's disease, resistance to medical therapy, and relapse?
    cigarette smoking
  10. What are the essentials of diagnosis for ulcerative colitis?
    • insidious onset
    • intermittent bouts of low grade fever, diarrhea, RLQ pain
    • RLQ mass and tenderness
    • perianal disease with abscess, fistulas
    • radiographic evidence
  11. What is the most common presentation for crohn's disease?
    • low grade fever
    • malaise
    • wt loss
    • loss of energy
    • possible diarrhea but it will be NON BLOODY and intermittent, cramping/steady RLQ or periumbilical pain
  12. What does the physical exam for crohn's disease show?
    • focal tenderness (usually RLQ)
    • possible palpable, tender mass in lower abdomen (thickened/matted loops of inflamed intestine)
  13. What are the abnormal radiological findings of crohn's disease of the jejunum?
    • irregular caliber of small intestine
    • poor distensibility
    • cobblestone appearance
    • areas of narrowing
  14. What are the extra intestinal manifestations of crohn's disease?
    • oral aphthous lesions are common
    • increased prevalence of gallstones due to malabsorption of bile salts from the terminal ileum
    • nephrolithiasis with urate or calcium oxalate stones
  15. What are the extra intestinal complications of inflammation secondary to crohn's disease?
    • acute arthropathy
    • sacroiliitis
    • ankylosing spondylitis
    • ocular complications
    • erythema nodosum
    • pyoderma gangrenosum
    • primary sclerosing cholangitis
    • nephrolithiasis
    • amyloidosis
  16. What do the laboratory findings reflect for crohn's disease?
    • inflammatory activity or nutritional complications
    • (poor correlation between lab studies and clinical picture)
  17. What are the lab findings of crohn's disease?
    • CBC (anemia): due to chronic inflammation, mucosal blood loss, iron deficiency, vitamin B12 malabsorption (terminal ileal inflammation/resection)
    • CBC (leukocytosis): inflammation/abscess formation (possibly secondary to corticosteroid therapy)
  18. The combination of tests for ASCA and pANCA may be helpful in clinical practice. How are these tests used in clinical practice to distinguish between ulcerative colitis and crohn's disease?
    • positive ASCA with a negative pANCA makes ulcerative colitis unlikely
    • positive pANCA with a negative ASCA makes crohn's disease unlikely
    • Note: ASCA and pANCA status must be interpreted in confunction with other clinical features and results of other diagnostic tests
  19. What are the special diagnostic studies used to help dx crohn's disease?
    • UGI series with small bowel follow through (all pts)
    • may use capsule endoscopy
    • barium enema/colonoscopy to evaluate the colon
  20. What are the endoscopic findings of crohn's disease?
    • aphthous ulcers
    • linear/stellate ulcers
    • strictures
    • segmental involvement with areas of normal appearing mucosa adjacent to inflamed mucosa
    • Note: may be impossible to distinguish UC from CD in 10% of cases
  21. What are the abnormal endoscopic findings of MUCOSAL features in crohn's disease?
    • ulcers (punched)
    • swollen mucosa
    • cobblestone
    • ulcers (linear)
    • pseudopolyps
  22. What clinical features suggest an abscess as a complication from crohn's disease? What test is used to confirm the diagnosis?
    • tender abdominal mass with fever and leukocytosis
    • emergent CT of abdomen
  23. What causes narrowing of the small bowel/intestinal obstruction in crohn's disease? What symptoms do patients report that point to this complication?
    • inflammation, spasm, fibrotic stenosis
    • postprandial bloating, cramping pains, loud borborygmus
  24. What type of fistulas can result in bacterial overgrowth with diarrhea, weight loss, and malnutrition?
    colon to small intestine (or stomach)
  25. What portion of patients with crohn's disease involving either the large or small bowel develop perianal disease? What are examples of these diseases?
    • one third
    • anal fissures, perianal abscesses, fistulas
  26. Patients with colonic crohn's disease are at increased risk for developing what disease? When should patients be screened for this?
    • colon carcinoma
    • screening recommended after 8 years of colitis
  27. What can cause malabsorption as a complication from crohn's disease? What issues lead to this process?
    • bacterial overgrowth
    • enterocolonic fistulas, strictures, extensive jejunal inflammation, prior surgical resections
  28. What is a complication of crohn's disease that is UNUSUAL?
    hemorrhage (unlike ulcerative colitis)
  29. What are the ddx and their symptoms for crohn's disease?
    • IBS: chronic cramping, abd pain, diarrhea (but xrays are normal with IBS)
    • appendicitis: acute fever and RLQ pain
    • intestinal lymphoma: fever, pain, weight loss, abnl small bowel radiographs (may mimic crohn's)
    • ulcerative colitis
    • ischemic colitis
    • enteric pathogens (TB, salmonella, campylobacter, etc)
    • caustic injury
  30. What are the overall goals in treatment of active crohn's disease?
    • symptomatic improvement (no specific therapy)
    • controlling disease process
    • tx must address specific problems of the individual patient
  31. How is active crohn's disease treated based on diet?
    • should be well balanced diet
    • trial of being off diary products (lactose intolerance common)
    • fiber supplementation (mainly COLONIC involvement)
    • low roughage diet for pts with OBSTRUCTIVE sxs (no raw fruits/veggies, popcorn, nuts, etc)
    • low fat diet with medium chain triglyceride supplements for pts with RESECTION of more than 100 cm of terminal ileum (fat malabsorption)
  32. How is treatment of active crohn's disease with chronic diarrhea managed with antidiarrheal medications?
    loperamide (2-4mg) up to 4 times a day
  33. What are the main indications for surgery in patients with crohn's disease?
    • intra-abdominal abscess
    • massive bleeding
    • obstruction with fibrous stricture
    • pts w/ active inflammation (unresponsive to medical therapy or who require chronic prednisone in doses >15mg/d)
    • Note: over half of pts will require at least one surgical procedure
  34. How long can a patient achieve dramatic relief of crohn's disease from surgical excision before the disease recurs?
    5-15 years
  35. What is believed to be almost as destructive as crohn's disease itself that has nothing to do with the physical GI tract itself?
    emotional damage due to pt's inability to lead a normal life
  36. What is the overall prognosis for pts with crohn's disease?
    • with proper medical & surgical tx the majority of pts are able to cope with it and lead productive lives
    • few pts die as a direct consequence of the disease itself
  37. What are the general considerations for ulcerative colitis?
    • in the majority of pts the extent of colonic involvement does not progress over time
    • in most pts disease is characterized by periods of symptomatic flare-ups and remissions
  38. What are the portions of patients with ulcerative colitis disease confined to different areas of the colon?
    • 1/3 have disease confined to rectosigmoid region (proctosigmoiditis)
    • 1/3 have disease extending to the splenic flexure (left sided colitis)
    • <20% extend more poximally (extensive colitis)
  39. In which patients is ulcerative colitis disease less severe?
    smokers (cessation may worsen disease)
  40. What are the essentials of diagnosis for ulcerative colitis?
    • bloody diarrhea
    • lower abdominal cramps & urgeny
    • anemia, low serum albumin
    • negative stool cultures
    • sigmoidoscopy
  41. What is the key to diagnosing ulcerative colitis?
  42. What is the hallmark symptom of ulcerative colitis?
    bloody diarrhea (clinically useful to classify pts as mild, moderate, or severe disease)
  43. What are the signs and symptoms of ulcerative colitis? What are some things the pt should be asked about?
    • ask about stool frequency and presence/amount of rectal bleeding
    • cramps
    • abdominal pain
    • fecal urgency
  44. What needs to be focused on during the physical examination in a pt with ulcerative colitis?
    volume status (orthostatic BP, pulse measurements, nutritional status)
  45. What are the findings during physical examination in pts with ulcerative colitis?
    • abdomen: tenderness, evidence of peritoneal inflammation
    • DRE: red blood may be present
  46. How can laboratory findings indicate disease severity in ulcerative colitis?
    degree of abnormality from hematocrit, sedimentation rate, and serum albumin
  47. What is the presentation of mild to moderate ulcerative colitis disease?
    • gradual onset of infrequent diarrhea (<5 BMs per day)
    • intermittent rectal bleeding & mucous
    • formed to loose stools
    • fecal urgency & tenesmus (rectal inflammation)
    • LLQ cramps relieved by defecation (common)
    • more severe diarrhea with frequent bleeding (moderate disease)
    • pain & tenderness may be present (not severe)
    • may have mild fever, anemia, hypoalbuminemia
  48. What is the presentation of severe ulcerative colitis disease?
    • >6 to 10 bloody BMs per day
    • severe anemia, hypovolemia, impaired nutrition with hypoalbuminemia
    • pain and tenderness present
    • "fulminant colitis" (subset of severe disease characterized by rapidly worsening symptoms w/ signs of toxicity)
  49. What procedure should NOT be performed in patients with severe ulcerative colitis and why?
    colonoscopy because of the risk of perforation
  50. What imaging study is used in pts with severe ulcerative colitis? What study is not used and why?
    • plain abdominal radiographs: looks for significant colonic dilation (ie, extensive gas in colon and small bowel)
    • barium enemas: are of little utility and may precipitate toxic megacolon in pts with severe disease
  51. What are the ddx for ulcerative colitis? How is ulcerative colitis distinguished from these other diseases?
    • infectious colitis
    • ischemic colitis
    • crohn's disease
    • Note: intial presentation of ulcerative colitis is indistinguishable from other causes of colitis (clinically and endoscopically) so the diagnosis is reached after EXCLUDING other known causes of colitis
  52. How is infectious colitis excluded as a diagnosis when evaluating for ulcerative colitis?
    • send stool specimens for routine bacterial cultures (salmonella, shigella, campylobacter)
    • ova and parasite (excludes amebiasis)
    • stool toxin assay for C difficile
  53. What does a mucosal biopsy help differentiate ulcerative colitis from?
    • amebic colitis
    • CMV colitis
    • gonorrhea, chlamydial infection, herpes, syphilis (sexually active pts w/ proctitis)
  54. What are the main treatment objectives for ulcerative colitis?
    • terminate acute, symptomatic attack
    • prevent recurrence of attacks
    • Note: treatment of acute UC is dependent on the extent of colonic involvement and severity of illness
  55. What is the acute treatment of ulcerative colitis confined to the rectum or rectosigmoid region (distal colitis)?
    Topical agents (mesalamine is the DOC and better than topical corticosteroids)
  56. What are the topical agents used to treat DISTAL ulcerative colitis and what are the formulations?
    • topical mesalamine (DOC): suppository for proctitis, enema for proctosigmoiditis
    • topical steroids: suppository for proctitis, enema for proctosigmoiditis
  57. How is distal ulcerative colitis treated if there is no improvement with topical mesalamine or steroids?
    • increase topical agent to BID
    • use topical 5 ASA AM and steroid PM
    • add oral 5 ASA agent
  58. How is mild to moderate ulcerative colitis generally treated?
    • 5 ASA: disease extending above the sigmoid colon
    • coritcosteroids: pts who don't respond to 5 ASA in 2-3 weeks (topical, systemic)
    • immunomodulating agents: 6 MP, anti-TNFs
  59. What percentage of patients with ulcerative colitis have severe colitis and how is it generally treated?
    • 10-15% have a more severe form of UC
    • hospitalization is generally required
  60. What are the indications for surgical therapy in patients with severe ulcerative colitis?
    • pts who fail to improve after 7-10 days of corticosteroid, anti-TNF, cyclosporine
    • pts w/ fulminant disease or toxic megacolon who worsen/fail to improve within 48-72 hrs (prevents perforation)
  61. What percentage of pts with ulcerative colitis develop toxic megacolon? What are the characteristics on radiographs?
    • <2% of pts develop megacolon
    • colonic dilation of more than 6cm on PLAIN FILMS with signs of toxicity
  62. Patients with ulcerative colitis proximal to the sigmoid colon have a markedly increased risk of developing what disease?
    colon carcinoma
  63. How often is a colonoscopy screening for colon carcinoma recommended in pts with extensive colitis?
    every 1-2 yrs beginning 8-10 years after diagnosis
  64. What are the ABSOLUTE indications for surgery in patients with ulcerative colitis?
    • severe hemorrhage
    • perforation
    • documented carcinoma
    • pts with fulminant colitis/toxic megacolon that does not improve within 48-72 hours
    • pts with dysplasia on surveillance colonoscopy
    • pts with refractory disease requiring chronic steroids to control symptoms
    • Note: surgery is required in about 25% of pts
  65. What surgical procedure provides a complete cure of ulcerative colitis disease?
    total proctocolectomy
  66. What is the general prognosis for pts with ulcerative colitis?
    • lifelong disease characterized by exacerbations and remissions readily controlled by medical therapy without the need for surgery in most patients
    • properly managed most UC pts lead close to normal productive lives
  67. What are the drugs used to treat inflammatory bowel disease (both entities are treated by these)?
    • 5 aminosalicylic acid (ASA)
    • corticosteroids
    • immune modulators (6 MP-mercaptopurine, azathioprine, methotrexate)
    • anti-TNF therapy
  68. Which topical agent is used in the active treatment of ulcerative colitis and crohn's disease and maintains remission during periods of disease inactivity?
  69. What are the formulations of 5-ASA currently available to tx IBD?
    • oral mesalamine: coated in various pH sensitive resins/timed release capsules
    • azo compounds: contain 5-ASA linked by an azo bond
    • topical mesalamine
  70. At what pH do mesalamine tablets dissolve and where is the 5-ASA released in the GI tract?
    • 7.0
    • terminal small bowel and proximal colon
  71. What are the 5-ASA azo compounds used to treat IBD? How do they work?
    • sulfasalazine, balsalazide, olsalazine
    • azo bond is cleaved by colonic bacteria
  72. Where does the oral mesalamine agent Pentasa release 5-ASA in the GI tract?
    released slowly throughout the small intestine and colon
  73. What are the side effects of sulfasalazine (azo compound)?
    • dose related: nausea, HA, leukopenia, oligospermia, impaired folate metabolism (always admin with folate)
    • allergic & idiosyncratic SE: fever, rash, hemolytic anemia, neutropenia, worsened colitis, hepatitis, pancreatitis, pneumonitis (inexpensive so its used anyway despite these SE)
  74. What formulations of mesalamine delivers much higher concentration of 5-ASA to the distal colon than oral compounds?
    • suppositories (500mg)
    • enemas (4g/60mL)
  75. What must you check before using mercaptopurine and azathioprine to treat refractory crohn's disease?
    thiopurine methyltransferase (TPMT) function due to immunosuppression
  76. What are the side effects of mercptopurine that occur in 10% of pts? What testing needs to be done on pts once therapy is started?
    • pancreatitis, bone marrow suppression, infections, allergies, potentially higher risk of neoplasm
    • CBC should be obtained weekly for 1 month then at least monthly
  77. What drug is used in patients who are intolerant of mercaptopurine? How can it be given? What are the side effects?
    • methotrexate
    • po, im, iv
    • SE: nausea, bone marrow suppression, hepatitis, and pneumonitis (check CBC & liver panel weekly, give folate supplement)
  78. What drugs are a major advance in refractory inflammatory bowel disease? What needs to be monitored while on these drugs?
    • anti-TNF (Infliximab)
    • monitor liver panel during therapy
  79. Discrete mass lesions that PROTRUDE INTO the intestinal lumen.
  80. What are the three major pathologic groups of colonic neoplasms?
    • mucosal neoplastic: adenomatous
    • mucosal non-neoplastic polyps: hyperplastic, juvenile, hamartomas, inflammatory
    • submucosal lesions: lipomas
  81. What type of polyps have significant disease risk? What percentage of polyps are this type?
    • adenomatous
    • 70%
  82. What is the only way to reliably distinguish an adenomatous from non-adenomatous polyp?
  83. Where do nonfamilial adenomatous polyps (adenomas) arise from? What percentage of adults over 50 yrs old have these polyps and why is this significant?
    • colonic epithelium
    • 35%
    • significant because colonic adenocarcinoma appears to start as adenomas
  84. What are the signs and symptoms of nonfamilial adenomatous polyps (adenomas)?
    • minimal or completely asymptomatic
    • anemia (possible chronic occult blood loss)
    • intermittent hematochezia (large polyps may ulcerate)
    • possible obstructive symptoms
  85. What are some non-invasive testing methods used to detect nonfamilial adenomatous polyps (adenomas)?
    fecal occult blood testing (FOBT)/guaiac stool testing/hemoccult (all the same test)
  86. What is the pathophysiology for colorectal cancer?
    • 5 yrs for undifferentiated tissue to progress to visible adenotomous polyps
    • 5 yrs for polyp to progress to grossly defined cancer
  87. How are nonfamilial adenomatous polyps (adenomas) treated?
    removal by electrocautery techniques
  88. What are the general considerations for colorectal cancer?
    • almost all are adenocarcinomas
    • about half (50%) are found within the rectosigmoid region
    • about one fourth (25%) are proximal in the cecum and ascending colon
  89. What are the risk factors associated with developing colorectal cancer?
    • age: 90% of cases in people >50 yrs
    • familial history of colorectal cancer: one of the most important factors accounting for 20-30% of CRC, risk is proportionate to the number of affected first degree relatives (1 relative=2x risk, 2 relatives=4x risk)
    • IBD: risk of CRC begins to rise about 7-10 yrs after onset of UC or CD, tx with 5-ASA and folate reduces risk in UC
    • dietary factors: red meats and high fat increase risk
    • chemoprevention: aspirin and NSAIDs decrease risk
    • race: african americans have higher rates of CRC than caucasian, may be genetic or socioeconomic
  90. What are the signs and symptoms of colorectal cancer?
    • presence of fecal occult blood
    • iron deficiency anemia
    • obstruction
    • constipation with occasional loose stools
    • rectal bleeding
  91. What is interesting about the physical exam findings in a patient with colorectal cancer?
    PE is usually normal
  92. What laboratory tests should be performed on patients with suspected colorectal cancer?
    • CBC
    • LFT
    • CEA (carcinoembryonic antigen)
  93. What studies are used to evaluate the colon for colorectal cancer?
    • barium enema
    • CT colonography
    • colonoscopy (diagnostic procedure of choice)
  94. What is the diagnostic procedure of choice for colorectal cancer?
  95. What are the differential diagnoses for colorectal cancer?
    • IBS
    • diverticular disease
    • ischemic colitis
    • IBD
    • infectious colitis
    • hemorrhoids
  96. What are the indications for a colorectal neoplasm?
    • change in bowel habits
    • hematochezia
    • unexplained iron deficiency anemia
    • occult blood in stools
  97. What is the treatment for colorectal cancer?
    • surgical resection
    • chemotherapy
    • radiation therapy
  98. What are two surgical resection resection techniques used to treat colorectal cancer?
    • segmental colectomy
    • hemicolectomy
    • Note: treatment depends on the extent and location of the tumor
  99. What improves overall survival and disease-free survival from colorectal cancer as an adjunct to surgical resection?
  100. What is done during the follow up after surgical resection of colorectal cancer?
    • colonoscopy 6 months to 1 year post surgery, then repeated every 3 years if there are no signs of recurrence
    • CEA (rising lvl is suggestive of tumor)
  101. What is the prognosis for colorectal cancer?
    • 35%: overall survival rate
    • 55% long term survival: if "curative" resection is done intitally
    • Note: stage of disease at presentation is one of the most important determinants of survival
  102. Why is it theoretically possible to prevent colon cancer with early detection and removal of adenomas during screening procedures (colonoscopy)?
    because virtually all colorectal cancers that arise are adenomas
  103. What are the 5 testing schedules used to screen for colorectal cancer?
    • annual FOBT
    • flexible sigmoidoscopy every 5 years
    • annual FOBT AND flex sig every 5 years
    • colonoscopy every 10 years
    • barium enema every 5 years
  104. What are the high risk patient groups that require screening COLONOSCOPY rather than Flex sig/BE?
    • pts with IBD more than 8-10 yrs duration
    • colon cancer families (hereditary nonpolyposis, hereditary polyposis)
  105. When should colon cancer screenings start for normal risk individuals according to ACS guidelines?
    50 yrs (men and women) with 1 of the 5 testing schedules
  106. What are the different hereditary polyposis syndromes?
    • familial adenomatous polyposis (FAP)
    • hamartomatous polyposis syndromes
    • hereditary nonpolyposis colorectal cancer (HNPCC)
  107. Which hereditary polyposis syndrome accounts for 0.5% of colon cancers, is autosomal dominant, and causes development of hundreds to thousands of adenomas in the colon beginning as early as age 10?
    • familial adenomatous polyposis (FAP)
    • Note: colon cancer is virtually inevitable by age 50 unless a prophylactic colectomy is done
  108. Which hereditary polyposis syndrome accounts for 0.1% of colon cancers, and is autosomal dominant? What is an example of this syndrome?
    hamartomatous syndromes (ie, peutz-jeghers syndrome)
  109. What are the characteristics of Peutz-Jeghers syndrome (hamartomatous syndrome)?
    • polyps throughout the GI tract
    • mucocutaneous pigmented macules on the lips, buccal mucosa and skin
  110. Which hereditary syndrome accounts for 3% of all colon cancers that develops earlier than 44 yrs of age (vs 65 yrs) and is mostly located on the right side (72%)?
    • hereditary nonpolyposis colorectal cancer (HNPCC)
    • Note: 60-80% of pts with HNPCC will develop colon cancer
  111. What are the Amsterdam II criteria for diagnosing HNPCC?
    • 3 family members must have been diagnosed with cancer associated with HNPCC
    • one of the 3 must be a first degree relative of the other two
    • at least two successive generations must be affected
    • at least one of these relatives must have been diagnosed before age 50
  112. What is the new "Bethesda criteria" for diagnosing HNPCC?
    • colorectal cancer <50 yrs
    • colorectal or HNPCC related tumor regardless of age
    • 2 or more 2nd degree relatives with colorectal or HNPCC related tumor
    • other specific tumors in pts <60 yrs
  113. What are the HNPCC related tumors?
    • endometrial
    • stomach
    • pancreas
    • ovary
    • ureter and renal
    • pelvis biliary tract
    • brain
  114. How should pts with HNPCC be screened for cancer?
    • colon cancer: begin at 21 yo, perform colonoscopy every 1-2 years
    • uterine/endometrial cancer: begin at 25-35 yo, transvaginal ultrasound, EMB, CA-125
    • send for genetic testing/counseling
  115. What are the general rules for colorectal cancer screening in patients with positive family history of CRC?
    • Risk factor: CRC in any FDR </= 60 yrs or >/= 2 FDR of any age
    • Age to begin screen: 40 or 10 yrs younger than youngest fam member with CRC
    • Method: colonoscopy
    • -------------------------
    • Risk factor: CRC in FDR >60 yrs
    • Age to begin screen: 40 yrs
    • Method: average risk options (1 of the 5 methods)
  116. What are the colonoscopy surveillance guidelines (risk factors & intervals)?
    • Risk: 1-2, <1 cm tubular adenomas
    • Surveillance interval: 5-10 years
    • ------------
    • Risk: >/=3, or >/=1 cm adenomas, or advance component (villous, high grade dysplasia)
    • Surveillance interval: 3 years
    • ------------
    • Risk: curative colon cancer resection
    • Surveillance interval: within 1 yr of surgery, repeat every 3 yrs if normal, then every 5 yrs if still normal
  117. Functional unit of the liver, consists of plates of hepatocytes hexagonally arranged around a central vein.
  118. Wide, leaky 'capillaries' within the liver that have no basement membrane and empty into the central vein.
  119. Explain the dual blood supply of the liver.
    • mostly via hepatic portal vein (nutrient-rich, deoxygenated blood)
    • some via hepatic artery (oxygenated)
    • both blood supplies mix in the sinusoids with drain into the central vein
    • blood leaves liver via hepatic vein which drains into the inferior vena cava (IVC)
  120. How does bile facilitate digestion?
    • emulsification
    • absorption of fat (via micelles)
    • solubilizes cholesterol
  121. What is bilirubin, and what are the two forms of bilirubin? Why is bile important in the excretion of bilirubin?
    • breakdown product of hemoglobin metabolism
    • direct (conjugated/water soluble), indirect (unconjugated/lipid soluble)
    • conjugated bilirubin is secreted into the bile canaliculus as part of bile and delivered to the small intestine, bacteria in the intestine metabolize bilirubin to other compounds which are eliminated either in feces or urine
    • Note: 90% of serum bili is UNCONJUGATED in healthy adults
  122. How is bile secreted?
    • bile ducts to,
    • right or left hepatic ducts to,
    • common hepatic duct which joins cystic duct of gallbladder forming the,
    • common bile duct which joins the,
    • pancreatic duct forming the,
    • hepatopancreatic ampulla
  123. What are the two mechanisms that control the secretion of bile?
    • parasympathetic stimulation: via vagus nerve
    • hormonal stimulation: fatty acids in duodenum stimulate CCK causing gall bladder to contract (empties), and Sphincter of Oddi relaxes; acidic chyme stimulates secretin which causes bile secretion
  124. What are gallstones usually made of and what causes them?
    • crystallized cholesterol
    • due to excess cholesterol or insufficient bile salts/lecithin in bile
  125. Yellowish coloration of sclera, skin, mucous membranes due to hyperbilirubinemia.
  126. What are the three main categories of jaundice?
    • prehepatic: increased bilirubin production (hemolytic disease)
    • hepatic: deficient bile production/bilirubin metabolism due to liver disease (i.e., hepatitis)
    • posthepatic: bile drainage blockage (ie, gallstones) or pancreatic/bowel cancer
  127. What LFT values are markers of liver injury NOT function?
    • AST
    • ALT
    • LDH
  128. Production of what liver marker elevates with hepatic injury, particularly OBSTRUCTION?
    alkaline phosphatase (ALP)
  129. What liver function test is an indicator of hepatic EXCRETION? Which test indicates the liver's ability to synthesize important PROTEINS? Which test indicates metabolism of VITAMIN K for normal blood coagulation?
    • bilirubin: excretion
    • albumin: protein synthesis
    • prothrombin time (PT): blood coag (vit K)
  130. What is the LFT pattern that indicates hepatocellular disease?
    elevations in AST & ALT predominate
  131. What is the LFT pattern that indicates cholestatic disease (retention of bile in liver)?
    alkaline phosphatase (ALP) elevations most noted
  132. What are the presenting symptoms for viral hepatitis?
    • prodrome of viral-like sxs (anorexia, N/V, malaise, aversion to smoking)
    • fever (low grade usually)
    • enlarged & tender liver
    • possible jaundice
    • normal to low WBCs
    • marked transaminase elevations EARLY in the course of disease
  133. What are the types of viral hepatitis?
    • Hep A, B, C, D, E, GB (HAV, HBV, HCV, HDV-delta agent, HEV, HGBV)
    • TT virus (TTV)/SEN-V
    • EBV, CMV, HSV (immunocompromised pts)
  134. What phase of viral hepatitis usually lasts a few weeks with complete clinical and laboratory recovery?
    • acute phase
    • Note: less than 1% will have acute fulminant course
  135. What are the clinical findings during the viral hepatitis prodromal phase?
    • malaise
    • myalgia
    • arthralgia
    • fatigue
    • anorexia
    • aversion to smoking
    • low grade fever
    • nausea/vomiting
    • RUQ/epigastric abdominal pain
  136. What are the clinical findings during the viral hepatitis icteric phase?
    • jaundice in some patients
    • worsening of prodromal sxs
  137. What are the clinical findings during the viral hepatitis convalescent phase?
    • increasing sense of well-being
    • return of appetite
    • resolved jaundice, abdominal pain, fatigue
  138. What is the general course of viral hepatitis?
    • acute illness: 2-6 weeks
    • complete clinical and lab recovery: 9 weeks (hep A), 16 weeks (hep B)
  139. What are the laboratory findings associated with viral hepatitis?
    • WBC normal to low
    • mild proteinuria
    • bilirubinemia
    • jaundice
    • strikingly elevated AST & ALT
    • marked PT prolongation (correlates with increased mortality)
  140. What is the only reliable way to diagnose a specific viral hepatitis type?
    serologic testing
  141. Which viral hepatitis causes an acute short lived illness with a very low mortality rate and no long term sequelae? How is it transmitted and what are some common sources?
    • Hepatitis A (HAV)
    • fecal-oral (ass to mouth!)
    • common sources are contaminated food or water
  142. When does virus excretion start with HAV? When does the virus clear from feces and when is a patient's blood and stool most infectious?
    • excretion: about 2 weeks before clinical illness
    • virus clears: after first week of physical symptoms
    • most infectious: during incubation (2-6 weeks) and in early illness
  143. Which viral hepatitis has a longer, more insidious onset along with a longer course of disease and slower recovery? How is it transmitted and what are some common sources?
    • Hepatitis B (HBV)
    • parenteral transmission, sexual contact
    • common sources include blood, saliva, semen, vaginal secretions
    • Note: mother may transmit to neonate (90% risk of chronic infection)
  144. What are some of the main characteristics and complications of HBV?
    • insidious onset
    • can progress to fulminant hepatitis and/or chronic hepatitis
    • known risk of cirrhosis and/or hepatocellular CA in chronic cases
  145. What are the three distinct antigen-antibody systems that are useful markers for diagnosing HBV?
    • HBs
    • HBc
    • HBe
  146. What antigen represents the first evidence of HBV infection, persists after acute illness associated with chronic hepatitis, and implies infectivity (establishes infection) if detected in blood?
  147. What antibody appears after clearance of HBsAg and/or VACCINATION, signals recovery, noninfectivity and protection against HBV?
    Anti-HBs (antibody to HBsAg)
  148. What appears shortly after HBsAg is detected, fills the serological gap in patients who have cleared HBsAg and have not yet made anti-HBs, can persist for 3-6 months, and reappears during flares of chronic HBV hepatitis?
    IgM anti-HBc (present in acute hepatitis diagnoses of HBV)
  149. What appears during acute HBV hepatitis but persists indefinitely regardless of whether or not a patient recovers or has chronic hepatitis?
    IgG anti-HBc (isolated with no other positive HBV serologic results is often a FALSE positive)
  150. Isolated levels of what antibody with no other positive HBV serological results can cause a false positive for HBV?
    IgG anti-HBc
  151. What antigen appears during the incubation period of HBV shortly after detection of HBsAg, and represents viral replication and infectivity?
    • HBeAg (secretory form of HBcAg)
    • Note: if it persists for >3 months there is an increased likelihood of chronic hepatitis
  152. What is the common serologic pattern of acute hepatitis B (HBV)?
    • (+/-) HBsAg
    • (-) anti-Hbs
    • IgM anti-HBc
    • (+/-) HBeAg
    • (-) anti-HBe
  153. What is the common serologic pattern of chronic HBV with active viral replication?
    • (+) HBsAg
    • (-) anti-HBs
    • IgG anti-HBc
    • (+) HBeAg
    • (-) anti-HBe
  154. What is the common serologic pattern of HBV recovery (immunity)?
    • (-) HBsAg
    • (+) anti-HBs
    • IgG anti-HBc
    • (-) HBeAg
    • (+/-) anti-HBe
  155. What is the common serologic pattern of HBV vaccination (immunity)?
    • (-) HBsAg
    • (+) anti-HBs
    • (-) anti-HBc
    • (-) HBeAg
    • (-) anti-HBe
  156. What is the common serologic pattern of a false positive for HBV infection?
    • (-) HBsAg
    • (-) anti-HBs
    • IgG anti-HBc
    • (-) HBeAg
    • (-) anti-HBe
  157. Which viral hepatitis is transmitted parenterally and is strongly associated with a chronic disease state? What are the currently known main sources?
    • Hepatitis C (HCV)
    • in the past it caused >90% of post-transfusion hepatitis cases, up to 50% are from IV drug use
    • Note: risk from sexual and maternal-neonate transmission is small
  158. What is the incubation period for HCV? What is the general clinical presentation of illness? What is the rate of chronic hepatitis associated with HCV?
    • incubation: averages 6-7 weeks
    • clinical illness: mild, asymptomatic, characterized by waxing & waning transaminase elevations
    • rate: >80%
  159. What is the diagnosis of HCV based on?
    • detection of antibodies to HCV
    • Note: testing of donated blood markedly reduces the risk of transmission
  160. Which viral hepatitis by itself is nonpathogenic (must be in conjunction with HBV to be pathologic)?
    Hepatitis D (HDV)
  161. Which viral hepatitis is enterically transmitted, is associated with large water-borne epidemics in many developing countries, usually causes a benign self-limiting illness and has a high mortality rate in pregnant women?
    Hepatitis E (HEV)
  162. Which viral hepatitis is percutaneously transmitted, causes long periods of chronic viremia, has been detected in IV drug users, hemodialysis pts, hemophiliacs, and pts with chronic hepatitis and does not appear to cause important liver disease?
    Hepatitis GB (HGBV)
  163. How is viral hepatitis A (HAV) prevented?
    • immune globulin: especially protective if given during incubation period
    • vaccines: 2 inactivated types available
  164. How is viral hepatitis B (HBV) prevented?
    • HBIG: protective if given within 7 days of exposure
    • HBV vaccine
    • universal precautions
    • safe sex
  165. What is the treatment for viral hepatitis B and C?
    • HBV: usually no treatment
    • HCV: interferon alpha, peginterferon, ribavirin if no clearance in 3 months
    • liver transplant: acute liver failure
  166. Viral hepatitis summary: blood and stool are infectious during incubation period and early illness, mortality is low, fulminant hepatitis is rare, chronic hepatitis does not occur, no carrier state.
    Hepatitis A (HAV)
  167. Viral hepatitis summary: transmission by infected blood or body fluids, presence of IgM and HBeAg and/or HBsAg indicates acute infection, risk of fulminant hepatitis is <1% but with a high mortality, 1-2% risk of chronic state.
    Hepatitis B (HBV)
  168. Viral hepatitis summary: transmission by infected blood, risk from sex is small, transfusion risk of HCV is now about 0.1% today, >50% of cases are due to intravenous drug abuse, >80% risk of chronic state.
    Hepatitis C (HCV)
  169. What are the most common causes of fulminant hepatitis?
    • intentional or accidental tylenol poisoning (most common of the most common)
    • drug reactions
    • viral hepatitis
    • poisonous mushrooms
    • many others
    • Note: mortality ~80%
  170. What is the definition of chronic hepatitis and what are the causes?
    • chronic inflammatory reaction of the liver lasting more than 3-6 months
    • caused by HBV, HCV, HDV, autoimmune, and meds
  171. Chronic hepatitis with insidious onset (about 40% of cases present as acute attack), generally a disease of young women but can occur in either sex and any age, and some cases follow a viral illness (HAV, EBV, or measles).
    autoimmune chronic hepatitis
  172. What are the signs and symptoms of autoimmune chronic hepatitis?
    • multiple spider nevi
    • cutaneous striae
    • hirsutism
    • hepatomegaly
    • markedly elevated AST/ALT (>1000 units/liter)
    • increased bilirubin
    • positive ANA or smooth muscle antibody
  173. What is the treatment for autoimmune chronic hepatitis?
    • prednisone w/ azathioprine or mercaptopurine
    • cyclosporine, tacrolimus, methotrexate (nonresponders)
    • Note: sx will usually improve promptly (80%)
  174. What is the treatment for viral chronic hepatitis?
    • PEGylated interferon alpha-2b
    • ribavirin
  175. What is the most common cause of cirrhosis in the US, outnumbering HCV 4 to 1 and a cause of death?
    alcoholic hepatitis
  176. What are some factors that play into developing alcoholic hepatitis?
    • dose related
    • 80% of pts have been drinking >5 yrs
    • women are more susceptible than men
  177. What are the clinical signs and symptoms for alcoholic hepatitis?
    • ranges from asymptomatic to,
    • N/V
    • jaundice
    • fever
    • tender hepatomegaly
    • ascites
  178. What are the laboratory findings for alcoholic hepatitis?
    • anemia
    • thrombocytopenia
    • elevated transaminase
    • elevated bilirubin
    • albumin decreased
    • GGT elevated in 50-75% of cases
    • AST>ALT (usually twice as high)
  179. What is the imaging used to exclude other diagnoses when evaluating alcoholic hepatitis? What testing method confirms the diagnosis?
    • ultrasound: r/o biliary obstruction, ascites
    • CT/MRI: r/o neoplasms, pancreatic disease
    • liver biopsy: confirms dx but isn't always done
  180. What is the treatment for alcoholic hepatitis?
    • STOP ALL ALCOHOL! (essential)
    • nutritional support
    • corticosteroids
    • pentoxifylline (anti-TNF)
  181. What is the prognosis for pts with alcoholic hepatitis?
    • grave if pt continues to drink
    • short term: if pt has liver dysfunction severe enough to prevent a biopsy there is a 42% 1 yr mortality, if its safe to do biopsy the mortality rate drops to 7%, mortality rate increases if there is progressive prolonged PT during hospitalization
  182. What needs to be seen on biopsy to make the diagnosis of alcoholic hepatitis?
    • fatty infiltrate
    • neutrophil infiltration
    • Mallory's hyalin
    • Note: clinically alcoholic hepatitis resembles acute viral hepatitis
  183. Why is drug and toxin induced liver disease difficult to diagnose and what can help establish this diagnosis?
    • mimics viral hepatitis or biliary tract obstruction
    • clinical history helps establish dx
  184. What characterizes toxin induced liver disease damage by direct hepatotoxic group?
    • dose related severity
    • latent period followed by exposure
    • occurs in all individuals
  185. What are idiosyncratic reactions of toxin induced liver disease?
    • sporadic
    • not related to dose
    • associated with features suggesting allergic reaction (fever, eosinophilia)
  186. What are the general considerations for nonalcoholic fatty liver disease (NAFLD)?
    • often asymptomatic
    • elevated aminotransferase (AMT) and/or hepatomegaly
    • macro and micro vesicular steatosis with/without inflammation and fibrosis on liver biopsy
  187. What are the causes of nonalcoholic fatty liver disease (NAFLD)/ steatosis ("fatty liver")?
    • obesity
    • DM
    • hypertriglyceridemia
    • steroids
    • Cushing's
  188. What are the signs and symptoms of nonalcoholic fatty liver disease (NAFLD)?
    • most are asymptomatic
    • RUQ tenderness
    • hepatomegaly
    • labs may be normal (elevated AST/ALT, ALT>AST in contrast to alcoholic hepatitis)
  189. What is the only way to assess the degree of inflammation and fibrosis in nonalcoholic fatty liver disease (NAFLD)? What is the histologic spectrum of NAFLD?
    • percutaneous biopsy
    • spectrum- fatty liver, isolated portal fibrosis, nonalcoholic steatohepatitis, cirrhosis
  190. What is the treatment for nonalcoholic fatty liver disease (NAFLD)?
    • weight loss
    • dietary fat restriction
    • exercise
    • metformin, other meds
  191. End result of hepatocellular injury that leads to both fibrosis and nodular regeneration throughout the liver, MAY be reversible if cause in removed (but generally irreversible).
  192. What are the most common symptoms of cirrhosis?
    • weakness
    • fatigability
    • weight loss
    • disturbed sleep
    • muscle cramps
  193. What are the signs and symptoms of advanced cirrhosis?
    • anorexia
    • weight loss, wasting
    • nausea, occasion vomiting
    • abdominal pain
    • menstrual abnormalities (usually amenorrhea)
    • impotence, loss of libido, sterility
    • painfully enlarged breasts in men
    • hematemesis is the presenting symptom in 15-25%
  194. What are the clinical signs of advanced cirrhosis?
    • liver enlargement
    • skin lesions
    • evidence of vitamin deficiencies (glossitis & cheilosis)
  195. What percentage of patients with advanced cirrhosis present with fever? What complications does this reflect?
    • 35%
    • alcoholic hepatitis, spontaneous bacterial peritonitis, cholangitis
  196. What percentage of patients with advanced cirrhosis present with splenomegaly? What are some physical findings on pts with splenomegaly?
    • 35-50%
    • dilated superficial veins of abdomen and thorax, rectal varices
  197. What are the laboratory findings in pts with cirrhosis?
    • anemia
    • coagulation abnormalities
    • modest elevates of AST and alkaline phosphatase (ALP), progressive elevation of bilirubin
    • low serum albumin, increased gamma globulin
    • Note: labs may be normal or minimally elevated in inactive cirrhosis
  198. What are EKG changes associated with cirrhosis?
    • prolonged QT interval
    • elevated troponin-I
  199. What test shows inactive cirrhosis (fibrosis with regenerative nodules), with no specific features to suggest the cause? When is this test contraindicated?
    • liver biopsy
    • CI in pts with prolonged prothrombin time (PT)
  200. What imaging study helps assess liver size and detect ascites?
    ultrasound (plain films seldom helpful)
  201. What are special examination techniques used to evaluate cirrhosis?
    • esophgogastroduodenoscopy (EGD)
    • laparoscopy
  202. What are the most common causes for cirrhosis of the liver?
    • alcohol abuse
    • chronic hepatitis B
    • chronic hepatitis C
  203. What are metabolic diseases that may lead to live cirrhosis?
    • hemochromatosis
    • Wilson's disease
    • primary & secondary biliary cirrhosis
    • congestive heart failure
    • hereditary hemorrhagic telangiectasia
  204. What are some complications of liver cirrhosis?
    upper GI bleed from varices (esophageal, rectal, gastric) and/or peptic ulcers
  205. What are special problems that arise due to liver cirrhosis and what diagnostic procedure is usually indicated?
    • ascites and edema
    • paracentesis
  206. What is the process for developing ascites in liver cirrhosis?
    • portal hypertension
    • hypoalbuminemia (decreased oncotic pressure)
    • peripheral vasodilation
    • impaired free water excretion (may develop hyponatremia)
  207. What is the treatment for ascites?
    • low sodium diet
    • fluid restriction
    • diuretics (spironolactone with lasix for pts who fail responding to salt restriction alone)
    • large volume paracentesis 4-6 liters (massive ascites & respiratory compromise, ascites refractory to diuretics, or intolerable diuretic side effects)
  208. What is the preferred peritoneovenous shunt used to treat refractory ascites?
    • transjugular intrahepatic portosystemic shunts (TIPS)
    • TIPS is alternative to surgical shunting in selected cases of variceal bleeding and provides short term control until liver transplant can be performed
  209. What are the signs and symptoms for spontaneous bacterial peritonitis caused by liver cirrhosis?
    • abdominal pain
    • increasing ascites
    • FEVER!
    • progressive encephalopathy (sxs may be mild)
  210. How is spontaneous bacterial peritonitis caused by liver cirrhosis diagnosed? What are the most common organisms involved? When should treatment be initiated?
    • cultures of ascites (highest yield)
    • E. coli and pneumococci
    • initiate tx while pending C&S results
  211. What antibiotic therapy is used to treat spontaneous bacterial peritonitis caused by liver cirrhosis?
    cefotaxime, 2g IV every 8 hours for at least 5-10 days
  212. The cause for this syndrome is unknown occurring in up to 10% of patients with cirrhosis and ascites.
    • hepatorenal syndrome
    • Note: histologically the kidneys are normal
  213. A condition of disordered central nervous system function resulting from liver failure.
    hepatic encephalopathy
  214. What is encephalopathy resulting from advanced liver cirrhosis associated with?
    • sleep reversal
    • asterixis
    • tremor
    • coma
    • dysarthria
    • delirium
    • drowsiness
  215. What is the etiology for hepatic encephalopathy?
    • ammonia (most readily common culprit)
    • bleeding into GI tract
    • protein digestion
  216. What are some precipitants for hepatic encephalopathy other than liver cirrhosis?
    • alkalosis
    • potassium deficiency induced by diuretics/narcotics
    • hypnotics
    • sedatives
  217. How is hepatic encephalopathy treated?
    • dietary protein should be COMPLETELY WITHHELD during acute episodes
    • control GI bleeding
    • purge blood from GI tract
  218. What drugs target ammonia producing flora in the treatment of hepatic encephalopathy?
    • neomycin sulfate, 0.5-1g orally every 6 or 12 hours for 5-7 days
    • lactolose
  219. What medications are contraindicated for treatment of hepatic encephalopathy?
    narcotics, tranquilizers, sedatives metabolized or excreted by the liver
  220. What types of anemia can be complications of liver cirrhosis?
    • iron deficiency anemia
    • macrocytic anemia (alcoholism)
  221. How are coagulopathies due to liver cirrhosis treated?
    • vitamin K for hypoprothrombinemia
    • transfusions with packed RBCs to replace blood loss
  222. What is the most common source of hemorrhage in liver cirrhosis?
    esophageal varices
  223. What are the triad of findings that identify hepatopulmonary syndrome due to liver cirrhosis?
    • chronic liver failure
    • increased alveolar-arterial gradient
    • intrapulmonary vascular dilation
  224. What are the absolute contraindications for liver transplantation?
    • sepsis
    • malignancy
    • advanced cardiopulmonary disease
  225. What are the relative contraindications for liver transplantation?
    • >70 yrs old
    • portal/mesenteric vein thrombosis
    • active drug/alcohol abuse
    • malnutrition
    • HIV infection
    • lack of pt understanding
  226. What is the point system classification of Child-Turcotte-Pugh in regards to ascites, encephalopathy, bilirubin, albumin and prothrombin time for liver cirrhosis prognosis?
    • ascites: none (1), slight (2), mod-severe (3)
    • encephalopathy: none (1), slight-mod (2), mod-severe (3)
    • bilirubin (umol/l): <2.0 (1), 2-3 (2), >3.0 (3)
    • albumin (g/dl): >3.5 (1), 2.8-3.5 (2), <2.8 (3)
    • prothrombin time (seconds increased): 1-3 (1), 4-6 (2), >6 (3)
  227. What are the points scales for Class A, B, and C in the Child-Turcotte-Pugh classification when determining the prognosis (1-2 survival rate) for liver cirrhosis?
    • Class A: 5-6 points (1 yr 100%, 2 yr 85%)
    • Class B: 7-9 points (1 yr 81%, 2 yr 57%)
    • Class C: 10-15 points (1yr 45%, 2 yr 35%)
  228. What is the 6 month survival rate in established cases of cirrhosis with severe hepatic dysfunction?
  229. Chronic disease of the liver that occurs in middle-aged women (40-60) caused by an autoimmune destruction of intrahepatic bile ducts and cholestasis, has insidious onset, and is often detected unexpectedly on discovering elevated alkaline phosphatase levels.
    primary biliary cirrhosis
  230. What are the signs and symptoms for primary biliary cirrhosis?
    • most are asymptomatic for years
    • onset in insidious and heralded by fatigue and pruritis
    • jaundice within 2 years of onset of pruritis
  231. What are the physical exam findings for primary biliary cirrhosis?
    • hepatosplenomegaly
    • xanthomatous lesions
    • excoriations
  232. What are the laboratory findings for primary biliary cirrhosis?
    • isolated elevated alkaline phosphatase
    • elevated cholesterol (esp HDL)
    • elevated bilirubin (later stages)
  233. What are the differential diagnoses of primary biliary cirrhosis?
    • chronic biliary duct obstruction
    • bile duct carcinoma
    • primary sclerosing cholangitis
    • cholestatic drug toxicity
    • chronic hapatitis
    • Note: occasional overlap in symptoms combining features of biliary cirrhosis and autoimmune hepatitis
  234. What are the treatments for primary biliary cirrhosis?
    • symptomatic treatment: cholestyramine, colestipol
    • ursodeoxycholic acid (Urso)
    • liver transplant for advanced disease
  235. Increased accumulation of iron stored as hemosiderin in the liver, pancreas, heart, adrenals, testes, pituitary, and kidneys. Occurs earlier in males (rarely recognized before 5th decade), and appears in affected women 10-20 years postmenopause.
  236. What are the signs and symptoms of hemochromatosis?
    • early: fatigue, arthralgias
    • late: arthropathy, hepatomegaly, occasionally skin pigmentation
    • general: cardiac enlargement, diabetes mellitus, impotence
  237. What are the laboratory findings for hemochromatosis?
    • mildly elevated LFTs (AST, alkaline phosphatase)
    • elevated plasma iron
    • elevated serum ferritin
  238. What can a CT and MRI show in a patient with hemochromatosis?
    changes consistent with iron overload of the liver
  239. What are the liver biopsy findings for hemochromatosis?
    • extensive iron deposition in hepatocytes, bile ducts, vessel walls, supporting tissues
    • dx confirmed by determining hepatic iron content in biopsy specimen
  240. How is hemochromatosis treated?
    • early dx and tx in the pre-cirrhotic phase is important
    • phlebotomy
    • chelation agents
  241. What is the general prognosis for patients with hemochromatosis?
    prognosis usually good with early detection and treatment
  242. Excessive deposition of copper in the liver and brain, may masquerade as chronic hepatitis, psych disorders, or neurologic disease. Potentially reversible with appropriate therapy which will also prevent neurologic and hepatic damage.
    Wilson's disease
  243. What is the etiology of Wilson's disease?
    • excessive absorption of copper from small intestine
    • decreased excretion of copper by liver
  244. What are the signs and symptoms of Wilson's disease?
    • tends to present as liver disease in adolescents and neuropsychiatric disease in young adults (rigidity/parkinsonian tremor)
    • hepatic signs range from elevated LFTs to cirrhosis and portal HTN
    • kayser-fleischer ring (brownish/gray-green ring in cornea)
  245. What is the diagnosis of Wilson's disease based on?
    • demonstrated increased urinary copper excretion
    • low serum ceruloplasmin
    • liver biopsy (may show acute/chronic hepatitis or cirrhosis)
  246. What is the treatment for Wilson's disease?
    • remove copper before it causes neurologic or hepatic damage
    • restriction of dietary copper
    • oral penicillamine (DOC), pyridoxine (vit B6)
    • Note: tx continues indefinitely
  247. What is the drug of choice to treat Wilson's disease?
    oral penicillamine
  248. What is the prognosis for pts with Wilson's disease?
    • without treatment is it ALWAYS FATAL
    • prognosis good in pts effectively treated before liver/brain damage
  249. Impaired conjugation of bilirubin by glucuronide that's an important benign cause of jaundice.
    gilbert's disease
  250. What is the physical presentation of patients with Budd-Chiari syndrome (hepatic vein obstruction)?
    • RUQ pain
    • ascites
  251. What is the screening test of choice for Budd-Chiari syndrome (hepatic vein obstruction)?
    doppler ultrasound
  252. How is Budd-Chiari syndrome (hepatic vein obstruction) treated?
    • correct underlying hematologic disorder
    • thrombolytics
    • TIPS
    • balloon angioplasty
    • liver transplant
  253. What are the signs and symptoms of pyogenic hepatic abscess?
    • fever
    • RUQ tenderness
    • jaundice
  254. What are the laboratory findings for pyogenic hepatic abscess?
    • leukocytosis (left shift)
    • elevated LFTs
    • positive blood cultures
  255. What are the etiologies of pyogenic hepatic abscess?
    • cholangitis (50%)
    • appendicitis (10%)
    • cryptogenic (10-40%)
  256. What are the antibiotics used to treated pyogenic liver abscesses? When is percutaneous, laparoscopic or open surgical drainage of the abscess indicated?
    • 3rd gen cephalosporins and metronidazole
    • if abscess if greater than 5cm or does not respond to antibiotics rapidly or at all
  257. Where are the majority of hepatocellular cancers (primary liver cancer) found? What are the most common risk factors for developing this?
    • 80% found in cirrhotic livers
    • HBV, HCV and alcohol are the most common risk factors
    • Note: primary liver cancer is not as common as metastatic cancer
  258. What are the symptoms of hepatocellular cancer (primary liver cancer)?
    • cachexia
    • weakness
    • weight loss
  259. What imaging studies demonstrate a hepatocellular cancer lesion?
    • MRI
    • CT
  260. What is the treatment for hepatocelluclar cancer (primary liver cancer)?
    • resection of solitary nodules 
    • transplant (may be impractical)
  261. What is the prognosis for pts with hepatocellular cancer?
    • 1 and 5 years respectively 23% and 5%
    • 56% for pts with localized resectable disease (1 and 5 yr)
  262. How are patients screened for hepatocellular cancer? How is it prevented?
    • check alpha fetoprotein and ultrasound every 6 months for pts with chronic HBV, cirrhosis from HCV or ETOH
    • prevent with mass HBV vaccinations, and HCV treatment
  263. What is the most common malignant liver tumor?
  264. What is a common site for metastasis?
  265. What is the histological appearance of metastasis tumors in the liver?
    resembles primary neoplasm
  266. The most common benign neoplasm of the liver, almost always asymptomatic in adults, and rarely requires treatment.
    cavernous hemangioma
  267. Benign liver neoplasm that occurs in all ages, is often asymptomatic and HYPERVASCULAR on CT/MRI, histologically reveals hyper plastic units of hepatocytes with "stellate" scar, treated with resection if symptomatic.
    focal nodular hyperlasia (FNH)
  268. Benign tumor of liver cells, usually cause by oral contraceptives, consists of a solitary nodule up to 15cm, occurs most commonly in 3rd & 4th decade, causes acute abdominal pain from necrosis, is hypovascular, does not affect LFTs (nl lvls) and is treated with surgical resection.
  269. What benign masses are a relatively common finding at surgery, involves the right liver lobe more than the left and rarely transform ins to a malignancy?
    solitary liver cysts
  270. The majority of liver cysts are ______ and lined by a single layer of ______.
    • unilocular
    • cuboidal cells
  271. A solid crystal deposit that forms in the gallbladder that varies in size and chemical structure (may be a small as a grain of sand or large as a golf ball).
    cholelithiasis (gallstones)
  272. What are the general risk factors for developing cholelithiasis (gallstones)?
    • obesity, esp women
    • rapid weight loss, esp obese people
    • crohn's disease
    • diabetes mellitus
    • cirrhosis
    • pregnancy
  273. What are the 5 Fs representing the risk factors for developing cholelithiasis (gallstones)?
    • female
    • fat
    • fertile
    • forty
    • flatulent
  274. How are gallstones classified? What are the two types?
    • according to chemical composition
    • cholesterol (80%)
    • calcium bilirubinate (<20%)
  275. What is the approach to treatment for asymptomatic cholelithiasis?
    generally no need for prophylactic cholecystectomy in an asymptomatic person
  276. What is the approach to treatment for "symptomatic" cholelithiasis?
    • usually have RUQ discomfort or pain (biliary colic)
    • laparascopic cholecystectomy (treatment of choice), but must be after careful consideration of other sources of symptoms
  277. What are the advantages and complications that can happen with a laparoscopic cholecystectomy?
    • advantage: minimal trauma
    • complication: bile duct injury in 0.1% of cases done by experienced surgeons
  278. Occurs when a stone becomes impacted in the cystic duct and inflammation develops behind the obstruction, and is associated with gallstones in over 90% of cases.
    cholecystitis (inflammation of gallbladder)
  279. What symptoms/pt presentations indicate the need to consider acalculous cholecystitis?
    • unexplained fever
    • RUQ pain within 2-4 weeks of major surgery
    • critically ill pt who had no oral intake for prolonged period
  280. What are the signs and symptoms of acute cholecystitis?
    • attack often preceded by large or fatty meal
    • sudden onset of severe, steady pain localized in epigastrium or right hypochondrium
    • may gradually subside over a period of 12-18 hrs (uncomplicated)
    • vomiting
    • RUQ abdominal tenderness (Murphy's sign)
    • guarding
    • rebound tenderness
    • fever
  281. What are the laboratory findings for acute cholecystitis?
    • WBC count usually high (12,000-15,000)
    • elevated alkaline phosphatase
    • elevated serum bilirubin
  282. What type of imaging study may show radiopaque gallstones (15% of cases)?
    plain films
  283. What imaging study do you need to get prior to surgical consultation for laparoscopic cholecystectomy?
    RUQ ultrasound
  284. What imaging scan is useful in demonstrating an obstructed cystic bile duct?
    99mTc hepatobiliary imaging (ie, hepatic iminodiacetic acid/HIDA)
  285. How is acute cholecystitis treated in the ER?
    • rest the abdomen: NPO, NG tube to decompress stomach
    • IV alimentation: surgical conclut
    • analgesics: surgical eval PRIOR to pain meds
    • antibiotics: surgeon may elect use to "cool down" infection, schedule surgery in 2-3 days
  286. It is usually best to defer surgery if possible in the presence of acute pancreatitis. Having said this, when is an operation (cholecystectomy) mandatory?
    when there is evidence of gangrene or perforation
  287. What are the signs/symptoms of gangrene of the gallbladder?
    increasing RUQ pain, guarding, leukocytosis
  288. What is Charcot's triad of symptoms that indicate cholangitis?
    • fever and chills
    • RUQ pain
    • jaundice
  289. What are the complications associated with acute cholecystitis?
    • gallbladder necrosis
    • cholangitis
  290. What is the prognosis for pts with acute cholecystitis?
    • mild acute: usually subsides but recurrences are common
    • symptomatic: definite indication for surgery
  291. Most common disorder that results from cholelithiasis, characterized by varying degrees of chronic inflammation on gross inspection or microscopic examination of the gallbladder (calculi are usually present).
    chronic cholecystitis
  292. What are the signs and symptoms of chronic cholecystitis?
    • recurrent episodes of biliary colic
    • pain may be referred to the inter scapular area/shoulder
  293. What are the physical examination findings for chronic cholecystitis?
    • nonspecific
    • abdominal tenderness
    • occasionally palpable gallbladder, and/or jaundice
  294. What are the routine lab studies performed to detect chronic cholecystitis?
    • WBC count
    • LFTs
    • amylase
  295. What can plain films reveal in a patient with chronic cholecystitis?
    • opacification of gallbladder caused by high concentration of calcium carbonate (limy bile)
    • radiopaque stones
  296. How is chronic cholecystitis treated?
    surgery (same as acute cholecystitis)
  297. What is the prognosis for patients with chronic cholecystitis?
    • mortality rate <1%
    • mortality rate 5-10% in the elderly
  298. Calculus in the common bile duct.
  299. What are the general considerations for choledocholithiasis?
    • common duct stone originate in gallbladder but may also form spontaneously in the common duct post cholecystectomy
    • stones are frequently "silent" since no symptoms result unless this is obstruction
  300. What are the essentials of diagnosis for choledocholithiasis?
    • PMH of biliary colic or jaundice
    • sudden onset of severe RUQ or epigastric pain
    • occasionally only painless jaundice
  301. What are the signs and symptoms of choledocholithiasis?
    • recurring attacks of RUQ pain that is severe and persists for hours
    • chills and fever
    • jaundice associated with episodic pain
    • cholangitis (charot's triad- fever/chills, RUQ pn,  jaundice)
    • acute suppurative cholangitis (reynold's pentad, chariot's triad PLUS sensorium & HOTN, endoscopic/surgical emergency)
  302. What are the laboratory findings for choledocholithiasis?
    • bilirubinuria
    • elevated serum bilirubin
    • elevated serum alkaline phosphatase
    • elevated serum amylase
  303. What imaging techniques are used to help dx choledocholithiasis?
    • ultrasonography
    • CT scan
    • radionuclide imaging bile flow
    • percutaneous transhepatic cholangiography (PTC)
    • endoscopic retrograde cholangiopancreatography (ERCP)
  304. What are the differential diagnoses of choledocholithiasis?
    • carcinoma of the pancreas, ampulla ov Vater or common bile duct
    • compression from extrinsic sources
    • chronic cholestatic liver disease
  305. What are the complications that can arise from choledocholithiasis?
    • biliary cirrhosis: from common duct obstruction lasting >30 days
    • hypoprothrombinemia: will respond to 10mg of parenteral vitamin K (unlike hepatocellular dysfunction hypoprothrombinemia)
  306. How is choledocholithiasis treated?
    • endoscopic papillotomy
    • followed by laparoscopic cholecystectomy
  307. Disease of the gallbladder that occurs in approximately 2% of all people operated on for biliary tract disease, is notoriously insidious and diagnosis is often made unexpectedly at surgery. Cholelithiasis is usually present.
    carcinoma of the gallbladder
  308. How does carcinoma of the biliary tract spread? What percentage of cancer deaths are due to this cancer in the USA?
    • direct extension into the live or peritoneal surface (initial manifestation)
    • only 3% of cancer deaths the USA, affects both genders equally, more prevalent in 50-60 yr olds
  309. What are the signs and symptoms of biliary tract carcinoma?
    • progressive jaundice
    • RUQ pain
    • anorexia
    • weight loss (with fever and chills)
    • Note: course is usually rapid deterioration with death occurring within a few months
  310. What are the physical exam findings with biliary tract carcinoma?
    • profound jaundice
    • hepatomegaly with liver tenderness
    • possibly ascites
    • pruritis and skin excoriations common
  311. What are the laboratory findings for biliary tract carcinoma?
    • conjugated hyperbilirubinemia (marked elevation)
    • elevated alkaline phosphatase
    • elevated serum cholesterol
    • normal/minimal increase of AST
  312. What are the most helpful diagnostic studies before surgery for biliary tract carcinoma?
    • percutaneous transhepatic cholangiography
    • endoscopic retrograde cholangiography with biopsy and cytologic specimens
  313. What is the treatment for biliary tract carcinoma?
    • curative surgery in young and fit patients if the tumor is will localized
    • however carcinoma of the biliary tract in curable by surgery in LESS than 10% of cases
    • palliation is the best treatment (poor prognosis)
  314. Retroperitoneal gland,, 12-15cm long posterior to stomach, with a head that fits into the curvature of the duodenum and tail adjacent to the spleen.
    • pancreas
    • Note: 99% exocrine acini, 1% endrocrine islets
  315. Describe the path pancreatic juices take through the pancreatic ducts.
    • pancreatic juice is secreted by acinar cells flow into ducts which empty into the,
    • pancreatic duct which joins the common bile duct to form the hepatopancreatic ampulla (of Vater) which empties into the,
    • duodenum and the major duodenal papilla and is controlled by,
    • Sphincter of Oddi
  316. What enzymes make up pancreatic secretions?
    • amylase
    • lipase
    • deoxyribonuclease & ribonuclease
    • sodium bicarbonate (acid buffer)
    • proteases (trypsin, chymotrypsin, carboxypeptidase, elastase)
  317. Thought to result from "escape" of activated pancreatic enzymes into surrounding tissues, most cases are related to biliary tract disease (passed gallstone) or heavy alcohol intake.
    acute pancreatitis
  318. What are the numerous other causes or associations for acute pancreatitis besides biliary tract disease?
    • hypercalcemia
    • hyperlipidemia
    • abdominal trauma (surgery)
    • drugs
    • viral infections (mumps)
    • ERCP
  319. What are the signs and symptoms for acute pancreatitis?
    • abrupt epigastric pain (steady and severe)
    • pain worse with walking and lying supine
    • better by sitting and leaning forward 
    • pain typically radiates to the back or right/left side
    • nausea & vomiting common
    • weakness, sweating, anxiety (severe attacks)
    • hx of alcohol intake/heavy meal before attack or similar episodes in the past
  320. What are the physical examination findings for acute pancreatitis?
    • upper abdomen tenderness often without guarding, rigidity, or rebound
    • abdominal distention
    • absent bowel sounds
    • fever
    • tachycardia
    • HOTN, pallor, cool clammy skin
    • mild jaundice common
    • Note: occasional upper abdominal mass, or acute renal failure
  321. Used in assessing the severity of acute alcoholic pancreatitis on presentation, and helps predict a severe course complicated by pancreatic necrosis.
    ranson's criteria
  322. In Ranson's criteria, 3 or more of what factors/findings need to be present on admission to predict a severe course complicated by pancreatic necrosis?
    • >55 yrs old
    • AST >250 IU/L
    • serum LDH >350 IU/L
    • blood glucose >200 mg/dL
    • WBC count >16,000
  323. The development of what issues following the first 48 hours of acute pancreatitis indicates a worsening prognosis?
    • HCT drops more than ten percentage points
    • BUN rises >5 mg/dL
    • arterial pO2 <60 mmHg
    • serum calcium <8 mg/dL
    • estimated fluid sequestration >6 L
    • base deficit over 4 meq/L
  324. What are the mortality rates for acute pancreatitis based on the number of Ranson's criteria?
    • 0-2: 1% (best)
    • 3-4: 16%
    • 5-6: 40%
    • 7-8: 100% (worst)
  325. What are the laboratory findings for acute pancreatitis?
    • leukocytosis (10,000-30,000)
    • proteinuria, casts (25% of cases)
    • glycosuria (10-20% of cases)
    • hyperglycemia
    • elevated serum bilirubin
    • elevated BUN
    • possibly elevated serum alkaline phosphatase
    • abnormal coagulation tests
    • elevated amylase and lipase within 24 hrs (90% of cases)
  326. What imaging study may show gallstones, a "sentinel loop" or linear focal atelectasis of the lower lobe of the lungs with or without pleural effusion in a pt with acute pancreatitis?
    plain films (non diagnostic findings)
  327. What imaging study is useful in detecting an enlarged pancreas, pseudocysts, helps in differentiating pancreatitis from other intra-abdominal catastrophes, and can show gas bubbles that imply infection (gas forming organisms) in a pt with acute pancreatitis?
    CT scan
  328. What imaging study is NOT reliable in acute cases of pancreatitis?
  329. What are the differential diagnoses of acute pancreatitis?
    • acutely perforated duodenal ulcer
    • acute cholecystitis
    • acute intestinal obstruction
    • renal colic
  330. What are some differential diagnoses for acute pancreatitis that can also show elevated serum amylase levels?
    • high intestinal obstruction
    • mumps not involving pancreas (salivary amylase)
    • ectopic pregnancy
    • narcotics
    • abdominal surgery
  331. What are the the complications of acute pancreatitis?
    • intravascular volume depletion (due to leakage of fluids in the pancreatic bed)
    • ileus
    • kidney failure
    • pancreatic necrosis
    • ARDS
    • pseudocysts
    • chronic pancreatitis
  332. How should necrotic tissue due to acute pancreatitis be aspirated? Why?
    • under CT guidance for gram stain and culture
    • because infected pancreatic necrosis is an absolute indication for operative treatment
  333. NOTE NOTE NOTE! A surgeon should be consulted in ALL cases of what disease?
  334. Encapsulated fluid collection (high enzyme content) that commonly appear in pancreatitis when CT scans are used to monitor the evolution of an acute attack.
  335. This develops in about 10% of cases of acute pancreatitis, causes permanent diabetes mellitus and pancreatic insufficiency.
    chronic pancreatitis
  336. How is acute pancreatitis generally managed?
    • in most patients it is mild and subsides spontaneously in several days
    • pancreatic rest program includes withholding food and liquid by mouth, bed rest, and pain control
  337. What is used to control pain with acute pancreatitis?
    • meperidine (or morphine)
    • Note: NPO until pt is mostly free of pain and has bowel sounds, then give clear liquids and gradually move to low fat diet
  338. How is severe pancreatitis managed?
    • IV fluids: may be considerable leakage of fluids during disease
    • monitoring in ICU: central venous pressure and blood gases at regular intervals
  339. What is the treatment for severe pancreatitis?
    • IV calcium gluconate: evidence of hypocalcemia with tetany
    • antibiotics: reserve for documented infections
    • C&S: blood, urine, sputum, pleural effusion if present
    • needle apsirations: areas of pancreatic necrosis (CT guidance)
  340. What laboratory values are mandatory to obtain as part of a close follow up in an ICU pt with severe pancreatitis?
    • WBC count
    • HCT
    • electrolytes
    • calcium
    • creatinine
    • BUN
    • serum AST & LDH
    • ABGs
    • Note: basically comprehensive metabolic panel, CBC and ABG
  341. What is a pancreatic abscess and how is it treated?
    • Infected pseudocysts associated with persisting pain, pancreatitis, or common duct obstruction
    • treated by prompt drainage usually through the flank
  342. What is the prognosis for pts with severe pancreatitis?
    • high esp with hepatic cardiovascular/renal impairment, or pancreatic necrosis develop
    • recurrences are common in alcoholic pancreatitis
  343. Pancreatitis that occurs most often in patients with alcoholism, can be hereditary or due to severe malnutrition, untreated hyperparathyroidism, or may be idiopathic.
    chronic pancreatitis
  344. What are the signs and symptoms of chronic pancreatitis?
    • persistent/recurrent episodes of epigastric and LUQ pain (referred to upper left lumbar region typical)
    • anorexia, nausea, vomiting, constipation, flatulence, weight loss are common
    • tenderness over pancreas
    • mild muscle guarding
    • paralytic ileus
    • attacks may only last a few hours or 2 weeks
    • steatorrhea may occur late in course
  345. What are the laboratory findings for chronic pancreatitis?
    • elevated serum amylase, lipase, bilirubin during acute attacks (nl amylase DOES NOT exclude diagnosis)
    • possible glycosuria
  346. What can imaging studies show in patients with chronic pancreatitis?
    • plain films: calcifications due to pancreaticolithiasis
    • CT: calcifications
    • ERCP: most sensitive, may show dilated ducts, stones, strictures, or pseudocysts
  347. What are the complications that can occur with chronic pancreatitis?
    • DM
    • pancreatic pseudocyst or abscess
    • common bile duct stricture
    • steatorrhea
    • malnutrition
    • peptic ulcer
    • narcotic dependency
  348. How is chronic pancreatitis with correctable coexistent biliary tract disease treat?
  349. What are some medical measures for managing chronic pancreatitis?
    • low fat diet
    • NO ALCOHOL (precipitates attacks)
    • pancreatic supplements for steatorrhea
    • insulin for associated DM
  350. What are the objectives of surgical treatment of chronic pancreatitis?
    • eradicate biliary tract disease
    • ensure free flow of bile into duodenum
    • eliminate obstruction of pancreatic duct
  351. What is the prognosis for pts with chronic pancreatitis?
    often leads to invalidism
  352. What are the essentials of diagnosis for carcinoma of the pancreas?
    • obstructive jaundice (may be painless)
    • enlarged gallbladder (may be painful)
    • upper abdominal pain with radiation to back, weight loss, thrombophlebitis (usually late manifestations)
  353. What are the general considerations for carcinoma of the pancreas?
    • carcinoma is most common neoplasm of the pancreas
    • carcinomas comprise 2% of all cancers and 5% of all cancer deaths
  354. What are the signs and symptoms of carcinoma of the pancreas?
    • pain
    • diarrhea
    • weight loss
  355. What are the laboratory findings for carcinoma of the pancreas?
    • mild anemia
    • serum amylase elevation
    • glycosuria
    • hyperglycemia
  356. What are the imaging studies used to detect carcinoma of the pancreas and how effective are they?
    • ultrasound: 70% sensitivity
    • CT: 80% sensitivity (can do guided biopsy but there is concern of seeding the track)
    • ERCP: 90% sensitivity (can safely get tissue samples)
  357. What is the approach of treatment for carcinoma of the pancreas?
    • resection attempted in 30% of patients (whipple procedure, pancreaticoduodenectomy)
    • chemotherapy (disappointing in metastatic cancer)
    • palliation for unresectable disease
  358. What is the general prognosis for pts with carcinoma of the pancreas?