INTERNAL MEDICINE BOARDS - PART 5 docx

GASTROENTEROLOGY & HEPATOLOGY 282 Ischemic Colitis Most common in the elderly and in patients with atherosclerotic or cardiovas- cular disease. Ranges from self-limited to life-threatening disease. Watershed areas (the splenic flexure and rectosigmoid junction of the colon) are the most common sites affected. Exsanguination and infarction are uncommon. SYMPTOMS/EXAM ■ Crampy left lower abdominal pain, hematochezia, nausea. ■ Abdominal exam is benign or reveals mild LLQ tenderness. DIFFERENTIAL IBD, infectious colitis, diverticulitis. DIAGNOSIS ■ Labs: Leukocytosis, anemia. ■ AXR: “Thumbprinting” is seen on the colon wall. ■ CT: Shows bowel wall thickening, luminal dilation, and pericolonic fat stranding. Vascular occlusion (e.g., mesenteric venous thrombosis) is un- common. ■ Flexible sigmoidoscopy: Contraindicated if peritoneal signs are present. Performed with minimal insufflation. Look for segmental changes sparing the rectum (due to preserved collateral circulation from hemorrhoidal plexus) and hemorrhagic nodules. Pale, dusky, ulcerative mucosa. TREATMENT ■ Correct hypotension, hypovolemia, and cardiac arrhythmias. ■ Minimize vasopressors; give broad-spectrum IV antibiotics. ■ Monitor for progression with serial exams and radiographs. ■ If there are signs of infarction (guarding, rebound tenderness, fever), lap- arotomy, revascularization, or bowel resection may be needed. PANCREATIC DISORDERS Acute Pancreatitis In the United States, > 80% of acute pancreatitis cases result from binge drinking or biliary stones; only 5% of heavy drinkers develop pancreatitis. Twenty percent of cases are complicated by necrotizing pancreatitis. Etiolo- gies are as follows: ■ EtOH and gallstones and, to a lesser extent, trauma. ■ Drugs: Azathioprine, pentamidine, sulfonamides, thiazide diuretics, 6-MP, valproic acid, didanosine. ■ Metabolic: Hyperlipidemia or hypercalcemia. ■ Mechanical: Pancreas divisum, sphincter of Oddi dysfunction, mass. ■ Infectious: Viruses (e.g., mumps) and, to a lesser extent, bacteria and para- sites (e.g., Ascaris lumbricoides). ■ Other: Scorpion bites, hereditary pancreatitis (an autosomal-dominant mutation of the trypsinogen gene), CF, pregnancy. Ischemic colitis typically affects the colonic “watershed” areas of the splenic flexure and rectosigmoid junction but spares the rectum. Ascaris lumbricoides causes up to 20% of cases of acute pancreatitis in Asia. Gallstones and alcohol are the main causes of pancreatitis in the United States. GASTROENTEROLOGY & HEPATOLOGY SYMPTOMS ■ Presents with sudden-onset, persistent, deep epigastric pain, often with ra- diation to the back, that worsens when patients are supine and improves when they sit or lean forward. ■ Severe nausea, vomiting, and fever are also seen. EXAM ■ Exam reveals upper abdominal tenderness with guarding and rebound. ■ Other findings include the following: ■ Severe cases: Distention, ileus, hypotension, tachycardia. ■ Rare: Umbilical (Cullen’s sign) or flank (Grey Turner’s sign) ecchy- mosis. ■ Other: Mild jaundice with stones or xanthomata with hyperlipidemia. DIFFERENTIAL Biliary colic, cholecystitis, mesenteric ischemia, intestinal obstruction/ileus, perforated hollow viscus, inferior MI, dissecting aortic aneurysm, ectopic pregnancy. DIAGNOSIS ■ Labs (see also Table 7.13): ■ Leukocytosis (10,000–30,000/μL); elevated amylase (more sensitive) and lipase (more specific). ■ There is no clinical use for serial amylase or lipase. ■ High serum glucose. ■ An ALT > 3 times normal suggests biliary stones over EtOH; an AST:ALT ratio > 2 favors EtOH. CRP declines with improvement. ■ Differential for elevated amylase: Pancreatitis, pancreatic tumors, chole- cystitis, perforation (esophagus, bowel), intestinal ischemia or infarction, appendicitis, ruptured ectopic pregnancy, mumps, ovarian cysts, lung can- cer, macroamylasemia, renal insufficiency, HIV, DKA, head trauma. Li- pase is usually normal in nonpancreatic amylase elevations. ■ AXR: May show gallstones, “sentinel loop” (an air-filled small bowel in the LUQ), and “colon cutoff sign” (abrupt ending of the transverse colon). ■ RUQ ultrasound: Reveals cholelithiasis without cholecystitis. Choledo- cholithiasis (common duct stones) are often missed or have passed. TABLE 7.13. Assessment of Pancreatitis Severity by Ranson’s Criteria a 24 HOURS: “GA LAW” 48 HOURS: “C HOBBS” Glucose > 200 mg/dL Ca < 8 mg/dL Age > 55 Hematocrit drop < 10% LDH > 350 U/L O 2 , arterial PO 2 < 60 mmHg AST > 250 U/L Base deficit > 4 mEq/L WBC > 16,000 /μL BUN rise > 5 mg/dL Sequestered fluid > 6 L a Mortality risk: 1% with 0–2 criteria; 16% with 3–4 criteria; 40% with 5–6 criteria; 100% with 7–8 criteria. 283 CT is prognostic in severe pancreatitis and is used to evaluate for necrotizing pancreatitis. Necrotizing pancreatitis warrants empiric antibiotics (imipenem). GASTROENTEROLOGY & HEPATOLOGY 284 ■ CT: Performed initially to exclude abdominal catastrophes. At 48–72 hours, exclude necrotizing pancreatitis. There is an ↑ risk of renal failure from contrast dye. TREATMENT ■ NPO with nasojejunal tube feeds or total parenteral nutrition with severe disease and anticipated NPO status for > 3–5 days. ■ Aggressive IV hydration. ■ Pain control with narcotics. Avoid morphine, as it ↑ sphincter of Oddi tone. ■ Broad-spectrum IV antibiotics (imipenem) for severe necrotizing pancre- atitis. ■ For gallstone pancreatitis (elevated serum bilirubin, signs of biliary sep- sis), perform ERCP for stone removal and cholecystectomy following re- covery but prior to discharge. COMPLICATIONS ■ Necrotizing pancreatitis: ■ Suspected in the setting of a persistently elevated WBC count (7–10 days), high fever, and shock (organ failure). ■ Has a poor prognosis (up to 30% mortality and 70% risk of complica- tions). ■ If infected necrosis is suspected, perform percutaneous aspiration. If or- ganisms are present on smear, surgical debridement is indicated. ■ Pancreatic pseudocyst: A collection of pancreatic fluid walled off by gran- ulation tissue. Occurs in approximately 30% of cases but resolves sponta- neously in about 50%. Drainage is not required unless the pseudocyst is present > 6–8 weeks and is enlarging and symptomatic. ■ Other: Pseudoaneurysm, renal failure, ARDS, splenic vein thrombosis (which can lead to isolated gastric varices). Chronic Pancreatitis Persistent inflammation of the pancreas with irreversible histologic changes, recurrent abdominal pain, and loss of exocrine/endocrine function. Marked by atrophic gland, dilated ducts, and calcifications, although all are late find- ings. Characterized by the size of pancreatic ducts injured; “big duct” injury is from EtOH. Risk factors include EtOH (amount and duration) and smok- ing. Associated with an ↑ risk of pancreatic cancer; 10- and 20-year survival rates are 70% and 45%, with death usually resulting from nonpancreatic causes. Etiologies are as follows: ■ EtOH (80%) and, to a lesser extent, hereditary pancreatitis (CF, trypsino- gen mutation). ■ Autoimmune: Rare and associated with diffuse enlargement of the pan- creas, ↑ IgG4, and autoantibodies; associated with other autoimmune dis- orders (e.g., Sjögren’s, SLE, 1° sclerosing cholangitis). ■ Obstructive: Pancreas divisum, sphincter of Oddi dysfunction, mass. ■ Metabolic: Malnutrition, hyperlipidemia, hyperparathyroid-associated hy- percalcemia. For persistent pancreatitis, no improvement on antibiotics (> 1 week), or suspicion of infected necrosis, consider CT with FNA to rule out infected necrosis, which requires surgical debridement. GASTROENTEROLOGY & HEPATOLOGY SYMPTOMS ■ Presents with recurrent, deep epigastric pain, often radiating to the back, that worsens with food intake and when patients lie supine and improves when they sit or lean forward. Episodes may last anywhere from hours to 2–3 weeks. ■ Also presents with anorexia, fear of eating (sitophobia), nausea/vomiting, and, later, weight loss and steatorrhea. EXAM ■ Exam is normal. Mild to moderate upper abdominal tenderness may be found during episodes. ■ Rarely, there may be a palpable epigastric mass (pseudocyst) or spleen (from splenic vein thrombosis). DIFFERENTIAL Biliary colic, mesenteric ischemia, PUD, nonulcer dyspepsia, inferior MI, perforation, IBS, drug-seeking behavior. DIAGNOSIS Diagnosis is as follows (see also Table 7.14): ■ No single test is adequate; routine labs are normal. Amylase and lipase are not always elevated during episodes. ■ Functional tests: ■ Often normal in “small duct” chronic pancreatitis; not ᮍ until 30–50% of the gland is destroyed. ■ Seventy-two-hour fecal fat test on 100-g/day fat diet: ᮍ in the pres- ence of > 7 g of fat in stool. ■ Stool chymotrypsin and elastase: Absent or low levels. ■ Secretin test: Most sensitive, but impractical. Give IV secretin and then measure pancreatic secretion via a nasobiliary tube. ■ Structural tests: Except for endoscopic ultrasound (EUS), imaging studies are insensitive, as architectural changes do not occur until late in the dis- ease course; diagnosis is improved with EUS +/− FNA. Pancreatic calcifi- cations are visualized on plain AXRs (30%); “big duct” injury is seen on CT. TABLE 7.14. Diagnosis of Chronic Pancreatitis “BIG DUCT”“SMALL DUCT” Seen on ultrasound or CT Yes No Seen on ERCP Yes Maybe Etiology EtOH Non-EtOH >> EtOH Loss of function (exocrine/endocrine) Common Less common Responsive to decompression Often Rarely (stenting, surgery) 285 Chronic pancreatitis of the “small duct” type may exhibit very subtle structural changes and is often associated with normal functional tests but marked symptoms. GASTROENTEROLOGY & HEPATOLOGY 286 ■ Histology: The gold standard, but impractical; obtained by EUS FNA. Reveals fibrosis, mixed lymphocyte and monocyte infiltrate, and architec- tural changes. TREATMENT ■ Alcohol abstinence. ■ Fat-soluble vitamins (vitamins A, D, E, and K); pancreatic enzymes. ■ Pain control with narcotics (avoid morphine) and celiac plexus injection. ■ ERCP with short-term pancreatic duct stenting and stone removal. ■ Surgical therapy is appropriate for intractable pain and failure of medical therapy; modalities include pancreatectomy, pancreaticojejunostomy (Puestow), and pseudocyst drainage. COMPLICATIONS ■ Malabsorption: Fat-soluble vitamins (A, D, E, and K); pancreatic en- zymes. ■ Metabolic bone disease: Osteopenia (33%) and osteoporosis (10%). Man- age with calcium, vitamin D, and bisphosphonates. ■ Other: Brittle DM, pancreatic pseudocyst, pseudoaneurysm, hemosuccus pancreaticus (bleeding from the pancreatic duct into the GI tract), splenic vein thrombosis, pancreatic cancer. BILIARY DISEASE Tables 7.15 and 7.16 classify diseases with jaundice and biliary tract disease. Cholelithiasis (Gallstones) and Acute Cholecystitis More common in women; incidence ↑ with age. In the United States, 10% of men and 20% of women > 65 years of age are affected; > 70% are cholesterol stones (see Table 7.17). Among patients with incidental asymptomatic gall- stones, only 15% have biliary colic at 10 years, and 2–3% have cholecystitis/ cholangitis. ■ Cholecystitis: The most common complication of cholelithiasis. More than 90% of cases are due to cholelithiasis with stone impacted in the cys- tic duct. Spontaneous resolution occurs in > 50% of cases within 7–10 days. ■ Acalculous cholecystitis (without gallstones): Usually seen in critically ill patients with no oral intake or following major surgical procedures; occurs after ischemia-related chronic gallbladder distention. SYMPTOMS ■ Cholelithiasis: Often asymptomatic or may present as follows: ■ Common: Biliary colic (crampy, wavelike RUQ pain), abdominal bloating, dyspepsia. ■ Uncommon: Nausea/vomiting (except in small bowel obstruction from gallstone ileus). ■ Cholecystitis: Sudden-onset, severe RUQ or epigastric pain that may radi- ate to the right shoulder, accompanied by nausea/vomiting and fever. Jaundice suggests common bile duct stones (choledocholithiasis) or com- pression of the common bile duct by an inflamed, impacted cystic duct (Mirizzi’s syndrome). Acalculous cholecystitis is generally seen in the critically ill with no oral intake or after major surgical procedures. GASTROENTEROLOGY & HEPATOLOGY 287 E XAM ■ Cholelithiasis: RUQ tenderness is commonly seen, but exam may be nor- mal. ■ Cholecystitis: RUQ tenderness and voluntary guarding; ᮍ Murphy’s sign (inspiratory arrest with palpation of the RUQ); fever; jaundice in < 25% of cases. DIFFERENTIAL ■ Choledocholithiasis, cholangitis, perforated peptic ulcer, acute pancreati- tis. ■ Diverticulitis (hepatic flexure, transverse colon), right-sided pneumonia. DIAGNOSIS ■ Cholelithiasis: Often an incidental finding on abdominal ultrasound or CT. ■ Cholecystitis: ■ Labs: Leukocytosis with neutrophil predominance; elevated total bilirubin (1–4 mg/dL) and transaminases (2–4 times normal) even without choledocholithiasis. Elevated alkaline phosphatase and amy- lase. ■ RUQ ultrasound: Less sensitive than HIDA scan but more readily available. Shows gallbladder wall thickening, pericholecystic fluid, and localization of stones. A radiographic Murphy’s sign (focal gall- TABLE 7.15. Classification of Jaundice TYPE OF HYPERBILIRUBINEMIA LOCATION AND CAUSE ↑ bilirubin production (e.g., hemolytic anemias, hemolytic reactions, hematoma, pulmonary infarction). Impaired bilirubin uptake and storage (e.g., posthepatitis hyperbilirubinemia, Gilbert’s syndrome, Crigler-Najjar syndrome, drug reactions). Hereditary cholestatic syndromes: Faulty excretion of bilirubin conjugates (e.g., Dubin-Johnson syndrome, Rotor’s syndrome). Hepatocellular dysfunction: ■ Biliary epithelial damage (e.g., hepatitis, hepatic cirrhosis). ■ Intrahepatic cholestasis (e.g., certain drugs, biliary cirrhosis, sepsis, postoperative jaundice). ■ Hepatocellular damage or intrahepatic cholestasis resulting from miscellaneous causes (e.g., spirochetal infections, infectious mononucleosis, cholangitis, sarcoidosis, lymphomas, industrial toxins). Biliary obstruction: Choledocholithiasis, biliary atresia, carcinoma of the biliary duct, sclerosing cholangitis, choledochal cyst, external pressure on the common duct, pancreatitis, pancreatic neoplasms. Unconjugated hyperbilirubinemia (predominant indirect-acting bilirubin) Conjugated hyperbilirubinemia (predominant direct-acting bilirubin) Adapted, with permission, from Tierney LM et al. Current Medical Diagnosis & Treatment, 44th ed. New York: McGraw-Hill, 2005: 630. GASTROENTEROLOGY & HEPATOLOGY 288 bladder tenderness under a transducer) has a 90% positive predictive value. Low sensitivity (50%) for choledocholithiasis. ■ HIDA scan: High sensitivity (95%) and specificity (90%). Assesses cystic duct patency; ᮍ in the setting of a ᮎ gallbladder uptake with preserved excretion into the small bowel. CCK stimulation assesses gallbladder contractility and aids in the diagnosis of acalculous chole- cystitis. TABLE 7.16. Diseases of the Biliary Tract CLINICAL FEATURES LABORATORY FEATURES DIAGNOSIS TREATMENT Asymptomatic None. Normal. Ultrasound. None. gallstones Symptomatic Biliary colic. Normal. Ultrasound. Laparoscopic gallstones cholecystectomy. Cholesterolosis Usually asymptomatic. Normal. Oral cholecystography. None. of gallbladder Adenomyomatosis May cause biliary colic. Normal. Oral cholecystography. Laparoscopic cholecystectomy if symptomatic. Porcelain gallbladder Usually asymptomatic; Normal. X-ray or CT. Laparoscopic high risk of gallbladder cholecystecomy. cancer. Acute cholecystitis Epigastric or RUQ Leukocytosis. Ultrasound, HIDA Antibiotics, pain, nausea, scan. laparoscopic vomiting, fever, cholecystectomy. Murphy’s sign. Chronic cholecystitis Biliary colic, constant Normal. Oral cholecystography, Laparoscopic epigastric or RUQ ultrasound (stones), cholecystectomy. pain, nausea. cholecystectomy (nonfunctioning gallbladder). Choledocholithiasis Asymptomatic or Cholestatic LFTs; Ultrasound (dilated Endoscopic biliary colic, jaundice, leukocytosis and ducts), ERCP. sphincterotomy and fever; gallstone blood cultures in stone extraction; pancreatitis. cholangitis; elevated antibiotics for amylase and lipase cholangitis. in pancreatitis. Adapted, with permission, from Tierney LM et al. Current Medical Diagnosis & Treatment, 44th ed. New York: McGraw-Hill, 2005: 663. GASTROENTEROLOGY & HEPATOLOGY 289 T REATMENT ■ Asymptomatic cholelithiasis: No specific treatment is indicated (even in DM). ■ Symptomatic cholelithiasis: ■ Consider prophylactic cholecystectomy. ■ Cholecystectomy can be postponed until recurrent symptoms are seen. ■ The risk of recurrent symptoms is 30–50% per year; the risk of com- plications is 1–2% per year. ■ Cholecystitis: ■ Antibiotics can be withheld in the setting of mild and uncompli- cated disease. ■ IV antibiotics: Provide coverage of gram-ᮎ enteric bacteria and ente- rococcus with antibiotics such as ampicillin and gentamicin (or ampi- cillin/sulbactam if the patient is ill). ■ Bowel rest. ■ Cholecystectomy should be performed after symptom resolution but prior to discharge. COMPLICATIONS ■ Gangrenous cholecystitis: The most common complication of cholecysti- tis (affects up to 20%), particularly in diabetics and the elderly. Patients ap- pear septic. ■ Emphysematous cholecystitis: 2° infection of the gallbladder with gas- forming organisms. More common in diabetics and the elderly; associated with high mortality. Gangrene and perforation may follow. ■ Cholecystenteric fistula: Uncommon. Stone erodes through the gallblad- der into the duodenum. Large stones (> 2.5 cm) can cause small bowel obstruction (gallstone ileus). ■ Mirizzi’s syndrome: Common bile duct obstruction by an inflamed im- pacted cystic duct. Uncommon. ■ Gallbladder hydrops. ■ Porcelain gallbladder: Intramural calcification. Associated with an ↑ risk of gallbladder cancer; cholecystectomy is indicated. TABLE 7.17. Types of Gallstones CHOLESTEROL BLACK PIGMENTED BROWN PIGMENTED Regional/ethnic Western countries, Pima Africa, Asia. Africa, Asia. predictors Indians, Caucasians >> blacks. Risk factors Age, female gender, Chronic hemolysis (sickle cell), Biliary infections, foreign pregnancy, estrogens, DM, cirrhosis, high-protein diet. bodies (stents, sutures), obesity, rapid weight loss, low-protein diet. elevated triglycerides, prolonged fasting, ileal disease (Crohn’s), ileal resection, CF. GASTROENTEROLOGY & HEPATOLOGY 290 Choledocholithiasis and Cholangitis Choledocholithiasis is defined as stones in the common bile duct. Cholangi- tis can be defined as biliary tree obstruction and subsequent suppurative in- fection. SYMPTOMS ■ Choledocholithiasis: Similar to cholelithiasis, except jaundice is more common in choledocholithiasis. Other symptoms include biliary colic (crampy, wavelike RUQ pain), abdominal bloating, and dyspepsia. May be asymptomatic. ■ Cholangitis: Similar to cholecystitis but frequently more severe, present- ing with fever, jaundice, and RUQ pain (Charcot’s triad). May also in- clude mental status changes and hypotension (Reynolds’ pentad). EXAM ■ Choledocholithiasis: Exam is normal or reveals mild RUQ tenderness along with jaundice. ■ Cholangitis: ■ Fever and RUQ tenderness with peritoneal signs (90%), jaundice (> 80%), hypotension, and altered mental status (15%). ■ Charcot’s triad (RUQ pain, jaundice, fever): Present in only 70% of patients. ■ Reynolds’ pentad (Charcot’s triad plus hypotension and altered mental status): Points to impending septic shock. DIFFERENTIAL ■ Choledocholithiasis: Mass lesions (e.g., pancreatic and ampullary carci- noma, cholangiocarcinoma, bulky lymphadenopathy), parasitic infection (e.g., ascariasis), AIDS cholangiopathy, 1° sclerosing cholangitis, recurrent pyogenic cholangitis. ■ Cholangitis: Perforated peptic ulcer, hepatitis, acute pancreatitis, appen- dicitis, hepatic abscess, diverticulitis, right-sided pneumonia. DIAGNOSIS ■ Choledocholithiasis: ■ Labs: No leukocytosis; elevated total bilirubin (> 2 mg/dL), transami- nases (2–4 times normal), and alkaline phosphatase. ■ RUQ ultrasound: Has low sensitivity (< 50%). ■ CT: Has higher sensitivity than RUQ ultrasound. ■ Cholangitis: ■ Labs: Leukocytosis with neutrophil predominance; elevated total bilirubin (> 2 mg/dL), transaminases (> 2–4 times normal), alkaline phosphatase, and amylase; bacteremia. ■ RUQ ultrasound: Shows dilation of the common bile duct and cholelithiasis. Less likely to visualize choledocholithiasis. ■ ERCP: Perform < 48 hours after presentation, ideally after IV antibi- otics and fluids. Requires sedation. Both diagnostic and therapeutic. ■ MRCP: Noninvasive and sensitive for diagnosis. ■ EUS: The most sensitive diagnostic study, but not readily available. ■ Percutaneous transhepatic cholangiography (PTHC): An alternative if ERCP is unavailable, unsafe, or unsuccessful. Does not require seda- tion. Charcot’s triad = RUQ pain, jaundice, and fever/chills. Reynolds’ pentad = Charcot’s triad plus hypotension and altered mental status. [...]... areas, supplement with the first HAV vaccine shot ALT HBeAg Anti-HBe HBV DNA HBsAg Anti-HBc IgM anti-HBc 0 1 2 3 4 5 6 F I G U R E 7 5 12 24 36 48 60 Months after exposure 120 Typical course of acute HBV (Reproduced, with permission, from Kasper DL et al Harrison’s Principles of Internal Medicine, 16th ed New York: McGraw-Hill, 20 05: 18 25. ) EXAM ■ GASTROE NTE ROLOGY & H E PATOLOGY ■ Acute: Icteric sclera,... long-acting nitrates Patients typically show low adherence/tolerance to β-blockers/nitrates Treat underlying disease Consider screening for hepatocellular carcinoma with ultrasound and serum AFP every six months TA B L E 7 2 2 CTP SCORE Child-Turcotte-Pugh Classification CHILD-PUGH CLASS THREE-YEAR SURVIVAL (%) 5 6 A > 90 7–9 B 50 –60 10– 15 C 30 308 ■ ■ Treat complications (see below) Liver transplantation:... (HEV), and contaminated food (shellfish and green onions) Labs: ■ HAV: Anti-HAV IgM (acute infection); anti-HAV IgG (prior exposure, vaccination); anti-HAV total measures IgM and IgG (acute infection, prior exposure, vaccination) ■ HEV: Anti-HEV IgM (acute infection); anti-HEV (prior exposure) 294 Jaundice ↑ ALT IgM anti-HAV IgG Anti-HAV Fecal HAV 0 F I G U R E 7 4 4 8 12 16 Typical course of acute HAV... and panacinar emphysema, pancreatic fibrosis, panniculitis Serum α1-antitrypsin concentration: For screening; α1-antitrypsin is an acute-phase reactant False-ᮍ tests may be obtained with inflammation (even if PiZZ) Serum α1-antitrypsin phenotyping: The screening and diagnostic test of choice Liver biopsy: Characteristic eosinophilic α1-antitrypsin globules are seen in the endoplasmic reticulum of periportal... two weeks of therapy Drug-Induced Hepatitis Elevated serum LDH suggests drug-induced hepatitis over viral hepatitis Ranges from subclinical disease with abnormal LFTs to fulminant hepatic failure Accounts for 40% of acute hepatitis cases in U.S adults > 50 years of age; for 25% of cases of fulminant hepatic failure; and for 5% of jaundice cases in hospitalized patients Drug-induced hepatitis can be... be seen in the neonatal period The incidence of liver disease at ages 20, 50 , and > 50 are 2%, 5% , and 15% , respectively, with males affected more often than females There is a high incidence of hepatocellular carcinoma in those with cirrhosis A high prevalence of HBV and HCV markers suggests synergistic liver injury Consider α1-antitrypsin deficiency in any adult who presents with chronic hepatitis or... ULN = upper limit of normal; AP = alkaline phosphatase; ASMA = anti–smooth muscle antibody; anti-LKM antibody = anti–liver/kidney microsome antibody ■ GASTROE NTE ROLOGY & H E PATOLOGY ■ ■ Steroid-sparing therapy: Lower-dose prednisone (30 mg QD); then taper over 4–6 weeks in combination with azathioprine 50 – 75 mg QD Treatment end points: Defined at the end of steroid taper ■ Remission: No symptoms; AST... incidence of bacterial infections (especially Vibrio, Yersinia, and Listeria spp) α1-antitrypsin protects tissues from protease-related degradation The deficiency is encoded on chromosome 14 and has an autosomal-codominant transmission The Z allele is the most common deficiency, particularly in those of Northern European descent α1-antitrypsin deficiency is severe when homozygous (e.g., PiZZ) and is intermediate... 1 25 mEq/dL ■ Large-volume paracentesis, portocaval shunt (TIPS), liver transplantation SBP prophylaxis: Fluoroquinolone or TMP-SMX Indicated for cirrhotics hospitalized with GI bleed (three days), ascites with total protein < 1 .5 g/dL (while hospitalized), or prior SBP (if the patient has ascites) SBP treatment: Do not wait for culture results to begin treatment Give cefotaxime or ceftriaxone IV × 5. .. Nutritional Recommendations 3 15 VITAMIN D 3 15 VITAMIN E 3 15 Weight Loss 3 15 Immunizations/Prophylaxis 316 INFLUENZA VACCINE 316 PNEUMOCOCCAL VACCINE 316 TETANUS VACCINE 316 ASPIRIN 316 Cancer Screening 317 CERVICAL CANCER 317 BREAST CANCER 317 COLON CANCER 317 PROSTATE CANCER 317 Sensory Impairment 317 VISION LOSS IN THE ELDERLY 317 HEARING LOSS IN THE ELDERLY 318 Cardiovascular Medicine 318 HYPERTENSION . Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 20 05: 1822.) Jaundice ↑ ALT IgM anti-HAV Fecal HAV IgG Anti-HAV 0481216 Hepatocellular carcinoma can occur. fibro- sis/cirrhosis. FIGURE 7 .5. Typical course of acute HBV. (Reproduced, with permission, from Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 20 05: . < 8 mg/dL Age > 55 Hematocrit drop < 10% LDH > 350 U/L O 2 , arterial PO 2 < 60 mmHg AST > 250 U/L Base deficit > 4 mEq/L WBC > 16,000 /μL BUN rise > 5 mg/dL Sequestered