Internal Medicine 2 EOR
#Surgical resection (whipple procedure) -is the only hope for a cure; however , only a minority of tumors are resectable. The prognosis is grim even after resection, with a 5 year survival rate of 10% #If the tumor is unresectable and biliary obstruction is present, perform PTC or ERCP with stent placement across the obstruction for palliation
Treatment of Pancreatic Cancer
#Nonoperative managment--appropriate if obstruction is incomplete and there is no fever, tachycardia, peritoneal signs, or leukocytosis -IV fluids to establish adequate urine output: add potassium to fluids to correct hypokalemia (which is typically present) -Nasogastric tube to empty stomach (gastric decompression) -Antibiotics #Surgery for complete obstruction, for partial obstruction that is persistent and/or associated with constant pain, or if strangulation is suspected. Perform an exploratory laparotomy with lysis of adhesions and restriction of any necrotic bowel
Treatment of Small Bowel Obstruction
#Medical A. Sulfasalazine (topical application as suppository)-- the mainstay of treatment. Preferred over topical steroids and can be sued as maintenance therapy. Remission rates as high as 93% have been reported -it is effective in maintaining remissions. 5-ASA (mesalamine) is the active component -5-ASA enemas can be used for proctitis and distal colitis B. Oral glucocorticoids--used when patients fail to respond to topical and oral 5-ASA therapy. If adquate clinical response is achieved, attempts to taper off of glucocorticoids should occur after 2 to 4 weeks. Can be used in conjunction with 5-ASA for pt with severe colitis C. TNF inhibitors (infliximab, adalimumab) and thiopurines (6-mercaptopurine, azathioprine), can be used in patients who do not respond to corticosteroids or for severe disease D. Immunosuppresive agents in patients with refractory disease may prevent relapse but are often not effective for acute attacks #Surgical-often curative (unlike Crohn's disease) and involves total colectomy. Indications for surgery include -severe disease that is debilitating, refractory, and unresponsive to medical therapy -Toxic megacolon risk (risk of perforation), obstruction (due to stricture), severe hemorrhage, perforation -Fulminant exacerbation that does not respond to steroids -Evidence of colon cancer or increased risk of colon cancer -Growth failure or failure to thrive in children -Systemic complications
Treatment of Ulcerative Colitis
Cholesterol stones
Yellow to green in color Associated with: -obesity, DM, HLD -multiple pregnancies, OCP use -Crohn's dz, ileal resection -advanced age -native american ancestry -cirrhosis -cystic fibrosis
Pigment stones
#Black in color Associated with: -hemolysis (e.g. sickle cell dz, thalassemia, hereditary spherocytosis, artificial cardiac valves, or alcoholic cirrhosis) #Brown in color -usually found in bile ducts and are associated with biliary tract infection #Mixed stones have components of both cholesterol and pigment stones, and account for the majority of stones
Chronic Mesenteric Ischemia
#Caused by atherosclerotic occlusive disease of main mesenteric vessels (celiac artery, superior and inferior mesenteric arteries) #Abdominal angina--dull pain, typically postprandial (when there is increased demand for splanchnic blood flow): analogous to anginal pain of CAD #Significant weight loss may occur due to abdominal angina #Mesenteric arteriography confirms the diagnosis #Surgical revascularization is definitive treatment and leads to pain relief in 90% of cases
Nonalcoholic Steatohepatitis (NASH)
#Histology of the liver is identical to that in patients with alcoholic liver disease, but these patients do not have a history alcohol use! #Associated with obesity, hyperlipidemia, diabetes mellitus (some patients have none of these) #usually asymptomatic and has a benign course (but cirrhosis develops in 10% to 15%) #Typically discovered on routine laboratory tests (mild elevation in ALT and AST) #Treatment is not clearly established
Pancreatic Cancer
#Most common in Elderly Patients (>75% of patients are >60 years old) #75% at head of the organ #Risk factors -cigarette smoking -chronic pancreatitis -diabetes -heavy alcohol use -exposure to chemicals benzidine and beta-naphthylamine #Prognosis is dismal: most patients die within months of diagnosis CLINICAL FEATURES #Abdominal pain (90% of patients)--may be vague and a dull ache #Jaundice #Weight loss #Recent onset of glucose intolerance, but DM is mild #Depression, weakness, fatigue #Migratory thrombophlebitis #Courvoisier sign (palpable gallbladder)-present in 30% of patients with cancer involving head of the pancreas; presents without paint DIAGNOSIS #ERCP is the most sensitive test in diagnosing pancreatic cancer #CT scan preferred for diagnosis and assessment of spread #Tumor markers -CA 19-9 -CEA
Diverticulitis
#Occurs when feces become impacted in the diverticulum, leading to erosion and microperfortaion #Can be complicated or uncomplicated CLINICAL FEATURES #Fever, LLQ pain, and leukocytosis #Alteration in bowel habits (constipation or diarrhea), vomiting, and sometimes a painful mass on rectal examination if inflammation is near the rectom DIAGNOSTICS #CT scan (abdomen and pelvis) w/ oral and IV contrast is the test of choice; it may reveal a swollen, edematous bowel wall or an abscess #Abdominal radiographs help in excluding other potential causes of LLQ pain, and can r/o ileus or obstruction (indicated by air-fluid levels, distension), and perforation (indicated by free air) #Barium enema and colonoscopy are contraindicated in acute diverticulitis due to the risk of perforation
Focal Nodular Hyperplasia
#This benign liver tumor without malignant potential occurs in women of reproductive age. There is no association with oral contraceptives #It is usually asymptomatic. Hepatosplenomegaly may be present #Treatment is not necessary in most cases
Cavernous Hemangioma
#Vascular tumors that are usually small and asymptomatic. They are most common type of benign liver tumor #As the size of the tumor increases (e.g. due to pregnancy or use of oral contraceptives), the symptoms increase and include RUQ pain or mass #Complications (uncommon unless tumor is very large) include rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF secondary to a large AV shunt, and gastric outlet obstruction #Diagnose w/ US or CT scan with IV contrast. Bx is contraindicated bc of risk of rupture and hemorrhage
Hepatocellular Adenoma
#benign liver tumor, most often sen in young women (15 to 40 years of age) oral contraceptive use, female sex, and anabolic steroid use are the main risk factors #pt may be asx; hepatocellular adenmoa may be discovered incidentally on abd imaging studies. RUQ pain or fullness may be present #malignant potential is very low (<1%). However, the adenoma may rupture, leading to hemoperitoneum and hemorrhage #diagnosis made by CT scan, US, or hepatic arteriography (most accurate but invasive)
#Portal HTN -bleeding (hematemesis, melena, hematochezia) -2/2 to esophagogastric varices is the most life-threatening complication of portal HTN -paracentesis can help in dx -tx the specific complication. Use transjugular intrahepatic portosystemic (TIPS) to lower portal pressure #Varices A. Esophageal/gastric: if present, prophylactic measures are indicated (such as nonselective Beta-blocker) -Clinical features include massive hematemesis, melena, and exacerbation of hepatic encephalopathy -initial tx is hemodynamic stabilization (give fluids to maintain BP) -IV abx given prophylactically -IV octreotide is initiated and continued for 3 to 5 days -Perform emergent upper GI endoscopy -Give nonselective Beta blockers (propanolol, timolol, nadolol) as long-term therapy to prevent rebleeding B. Rectal hemorrhoids C. Caput medusae #Ascites -accumulation of fluid in the peritoneal cavity due to portal HTN (increased hydrostatic pressure) and hypoalbuminemia (reduced oncotic pressure). Ascites is the most common complication of cirrhosis. Patients without portal htn do not develop ascites -clinical features: abdominal distension, shifting dullness, and fluid wave -abdominal ultrasound can detect as little as 30mL of fluid -diagnostic paracentesis determines whether ascites is due to portal HTN or another process *indications include new-onset ascites, worsening ascites, and suspected spontaneous bacterial peritonitis *examine cell count, ascites albumin, gram stain, and culture to r/o infection (e.g. SBP) *measure the serum ascites albumin gradient. If it is >1.1g/dL, portal HTN is very likely. If <1.1 g/dL, portal HTN is unlikely, and other causes must be considered -treatment: low sodium diet and diuretics (spironolactone to reduce accumulation of fluid, and furosemide to prevent hyperkalemia caused by sprionolactone) -perform therapeutic paracentesis if tense ascites, shortness of breath, or early satiety is present -peritoneovenous shunt or tips to reduce portal HTN #Hepatic encephalopathy -Toxic metabolites (there are many, but ammonia is believed to be most important) that are normally detoxified or removed by the liver accumulate and reach the brain -occurs in 50% of all cases of cirrhosis with varying severity -precipitants include alkalosis, hypokalemia (e.g. due to diuretics), sedating drugs (narcotics, sleeping medications), GI bleeding, systemic infection, and hypovolemia -Clinical features: deceased mental function, confusion, poor concentration, even stupor or coma; asterixis, rigidity, hyperreflexia, fetor hepaticus (musty odor or breath) -Treatment: *Lactulose prevents absorption of ammonia-metabolism of lactulose by bacteria in the colon favors formation of NH4+, which is poorly absorbed from GI tract, thereby promoting excretion of ammonia *Rifaximin (abx): kills bowel flora; so decreases ammonia production by intestinal bacteria *Diet-limit protein to 30 to 40g/day #Hepatorenal Syndrome -indicates end-stage liver disease -progressive renal failure in advanced liver disease, secondary to renal hypoperfusion resulting form vasoconstriction of renal vessels -often precipitated by infection or diuretics -this is a functional renal failure--kidneys are normal in terms of morphology, and no specific causes of renal dysfunction are evident. This condition does not respond to volume expansion -clinical features: azotemia, oliguria, hyponatremia, hypotension, low urine sodium (<10mEq/L) -Treatment: liver transplantation is the only cure. In general, the prognosis is very poor, and the condition is usually fatal without liver transplantation #SBP: infected ascitic fluid; occurs in up to 20% of patients hospitalized for ascites -usually occurs in pt with ascites caused by end-stage liver disease; associated with high mortality rate (20% to 30%) -has a high recurrence rate (up to 705 in first year) -Etiologic agents: escherichia coli (mc), klebsiella, streptococcus pneumoniae -clinical features: abdominal pain, fever, vomiting, rebound tenderness, SBP may lead to sepsis -Diagnosis is established by paracentesis and examination of ascitic fluid for WBCs (especially PMNs), Gram stain w/ culture, and sensitivities (WBC>500, PMN>250) -positive ascites culture; culture-negative SBP is common as well -Treatment: broad spectrum abx therapy: give specific abx once organism is identified, clinical improvement should be seen in 24 to 48 hours. Repeat paracentesis in 2 to 3 days to document a decrease in ascitic fluid PMN (<250) #Hyperestrinism-due to reduce hepatic catabolism of estrogens -spider angiomas--dilated cutaenous arterioles with central red sot and reddish extensions that radiate outward like a spider's web -palmar erythema -gynecomastia -testicular atrophy #Coagulopathy-secondary to decreased synthesis of clotting factors -prolonged prothrombin time (PT); PTT may be prolonged with severe disease -Vitamin K supplementation ineffective bc it cannot be used by diseased liver -treat coagulopathy with fresh frozen plasma #Hepatocellular Carcinoma (HCC)- present in 10% to 25% of patients with cirrhosis. All patients with cirrhosis should be screened for HCC, most commonly with serum AFP measurement with liver ultrasound every 6 months
Complications of Cirrhosis
Cirrhosis
CAUSES #Alcohol liver disease-MCC -refers to a range of conditions from fatty liver (reversible, due to acute ingestion) to cirrhosis (irreversible) -15% to 20% of heavy drinkers develop alcoholic cirrhosis #Chronic hepatitis B and C infections #Nonalcoholic steatohepatitis (NASH) #Drugs (e.g. acetaminophen toxicity, methotrexate) #Autoimmune hepatitis #Primary biliary cirrhosis (PBC), secondary biliary cirrhosis #Inherited metabolic diseases (e.g. hemochromatosis, Wilson disease) #Hepatic congestion secondary to R sided heart failure, constrictive pericarditis #Alpha1-antitrypsin (AAT) deficiency #Hepatic veno-occlusive disease-can occur after bone marrow transplantation CLINICAL FEATURES -some patients have no overt clinical findings, especially in early disease -patients may have signs or symptoms suggestive of one or more of the complications of cirrhosis
Constipation
CAUSES #Diet-lack of fiber #Medications-anticholinergic drugs (antipsychotics), antidepressants, narcotic analgesics, iron, calcium channel blockers, aluminum or calcium containing antacids, laxative abuse, and dependence #IBS #Obstruction-colorectal cancer (CRC), anal stricture, hemorrhoids, anal fissure #ileus, pseudo obstruction #anorectal problems-hemorrhoids, fissures #Endocrine/metabolic causes: hypothyroid, hypercalcemia, hypokalemia, uremia, dehydration #NM disorders-Parkinson's dz, MS, CNS lesions, scleroderma, DM (autonomic neuropathy) #Congenital disorders-Hirschprung disease DIAGNOSIS #Lab tests that may be necessary include: TSH, serum calcium levels, CBC (if colon cancer is suspected), and electrolytes (if obstruction is suspected) #Always attempt to r/o obstruction -if H&P is suggestive of obstruction, order abdominal films -consider flexible sigmoidoscopy in select cases (if an obstructing colorectal mass is suspected) #A rectal examination may help identify fissures, hemorrhoids, fecal impaction, or masses #If no cause is found after the above measures, and conservative tx does not help, more specialized tests are available--for example, radiopaque marker transit study, anorectal motility study
Viral Hepatitis
CLINICAL FEATURES #Classified as acute (<6 months of liver inflammation) or chronic (>6 months of persistent liver inflammation #Acute hepatitis has a wide spectrum of clinical presentations, ranging from virtually ASx to fulminant liver failure a. General clinical features -jaundice, look first in sclera -dark-colored urine may be present (due to conjugated hyperbilirubinemia) -RUQ pain -N/V -Fever and malaise -Hepatomegaly may also be present b. In severe cases, acute hepatitis may result in liver failure and tis complications-->fulminant hepatitis (uncommon) and may be life threatening. Occurs more commonly in hepatitis B, D, and E than in other types. Complications include -hepatic encephalopathy-asterixis and palmar erythema -hepatorenal syndrome -bleeding diathesis-this occurs only when liver function is very compromised c. Sometimes acute hepatitis may only present with transient flu-like symptoms such as fever, myalgias, and malaise d. acute HBV may also present with serum sickness-like illness e. hepatitis C typically does not cause significant acute illness #Chronic Hepatitis also has a wide variety of presentations. Some patients are asymptomatic ("chronic carriers") and may only present with w/ late complications of hepatitis such as cirrhosis or hepatocellular carcinoma -chronic hepatis occurs after acute hepatitis in 1% to 10% of patients with HBV and ?80% patients with HCV -it is categorized based on the grade of inflammation, the stage of fibrosis, and the etiology of disease -the risk of developing cirrhosis or HCC is 25% to 40% in patients with chronic HBV and 10% to 25% in patients with chronic HCV DIAGNOSIS #Serum serology PCR to detect viral RNA to diagnose HCV #LFTs-elevation of serum transaminases is not diagnostic, but LFTs are helpful. -ALT (SGPT) is typically elevated more than AST (SGOT) for all forms of viral hepatitis (the opposite of alcoholic hepatitis) -In acute hepatitis, ALT is usually >1,000. It is generally not as high as in drug-induced hepatitis -In chronic HBV, ALT can also be >1,000, but this varies. In chronic HCV, ALT is generally lower than this due to destruction of hepatocytes from longevity of disease
Appendicitis
CLINICAL FEATURES #Symptoms -abdominal pain--classically starts in the epigastrium, moves toward umbilicus and then to the RLQ. With distension of the appendix, the parietal peritoneum may become irritated, leading to sharp pain -anorexia always present -N/V typically follow pain #Signs -Tenderness in RLQ (maximal tenderness at McBurney point: two-thirds of the distance form the umbilicus to the right anterior superior iliac spine -Rebound tenderness, guarding, diminished bowel sounds -low-grade fever (May spike if perforation occurs) -Rovsing sign: deep palpation in LLQ causes referred pain in RLQ -Obturator sign: pain in RLQ when flexed right thigh is internally rotated when patient is supine DIAGNOSIS: -Clinical -Lab findings (mild leukocytosis) are only supportive -Imaging studies may be helpful if dx uncertain or in atypical presentations *CT scan (sensitivity 98% to 100%)-lowers the false-positive rate significantly *Ultrasound (sensitivity to 90%)
Cholelithiasis
CLINICAL FEATURES -Asx, incidental finding -biliary colic, 2/2 to temporary obstruction of the cystic duct in the GB -RUQ pain/epigastric pain may be mild, moderate, or severe -Pt classically report pain after eating and at night -Boas sign-referred right subscapular pain of biliary colic COMPLICATIONS -Cholecystitis -Choledocolithiasis -Gallstone ileus -Malignancy DIAGNOSIS -RUQ ultrasound has high sensitivity and specificity (>95%) for stones >2mm -CT scan and MRI are alternatives
#Pancreatic Necrosis -Sterile: infxn may develop, should be monitored in ICU, if >30% involvement ppx is indicated -Infected: multiple organ failure in 50% of cases , high mortality, surgical debridement and abx are indicated -only way to distinguish is via CT-guided percutaneous aspiration with gram stain/culture of the aspirate #Pancreatic Pseudocyst -encapsulated fluid collection that appears 2-3 weeks after an acute attack--unlike true cyst, it lacks an epithelial lining -complications include: rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cysts, and pancreatic ascites -may impinge on adjacent abdominal organs if large enough, may cause compression of the CBD DX with CT scan Tx: Observation if <5cm, Surgical or percutaneous drainage if >5cm #Hemorrhagic Pancreatitis -characterized by cullen sign, grey turner sign, and fox sign -CT scan with IV contrast is the study of choice #Adult respiratory distress syndrome--a life threatening complication with high mortality rate #Pancreatic ascites/pleural effusion-the MCC is inflammation of peritoneal surfaces #Ascending cholangitis--d/t gallstone in the ampulla of Vater, leading to infection of biliary tract; see section on cholangitis #Pancreatic abscess (rare)--develops over 4 to 6 weeks and is less life threatening than infected pancreatic necrosis
Complications of pancreatitis
Achalasia
GENERAL CHARACTERISTICS #Acquired motor d/o of esophageal smooth muscle in which the LES fails to completely relax w/ swallowing, and abn peristalsis of esophageal body replaces normal peristalsis #Absolute criteria for diagnos -incomplete relaxation of the LES -Aperistalsis of esophagus CAUSES #idiopathic #adenocarcinoma of proximal stomach is second most common cause #Worldwide, Chagas dz is important cause CLINICAL FEATURES #Dysphagia (odynophagia i less common) -equal difficulty swallowing solids and liquids (in contrast to esophageal cancer, in which dysphagia for solids starts first, than later for liquids -pt tend to eat slowly and drink a lot of water to wash down food. Also, they may twist their body, extend their neck, or walk about the room in an effort to force food into their stomach -exacerbated by fast eating and emotional stress #Regurgitation -food gets "stuck" in esophagus and then comes back up -regurgitation may lead to aspiration #Chest pain #Weight loss #Recurrent pulmonary complications secondary to aspiration, which may cause lung abscess, bronchiectasis, or hemoptysis DIAGNOSIS #Barium swallow-"bird's beak"-beak-like narrowing of distal esophagus and a large, dilated esophagus proximal to the narrowing #Upper GI endoscopy--to r/o secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal cancer #Manometry--to confirm dx; reveals failure of LES relaxation and aperistalsis of esophageal body
Ulcerative Colitis
GENERAL CHARACTERISTICS #Chronic inflammatory dz of colon and rectal mucosa #may occur at any age #Distribution: UC involves the rectum in all cases and can involve the colon either partially or entirely, but is always continuous. There are no skip lesions as are seen in crohn's -40% rectum and left colon -small bowel not usually resolved but 10% have backwash ileitis #Course is unpredicatble and variable and is characterized by periodic exacerbation and periods of complete remission. Less than 5% of patients have an initial attack without any occurrence CLINICAL FEATURES #Hematochezia-bloody diarrhea #Abdominal pain #Bowel movements are frequent but small #Fever, anorexia, and weight loss (severe cases) #Tenesmus (rectal dry heaves) #Extraintestinal symptoms (e.g. jaundics, uveitis, arthritis, skin lestions) DIAGNOSIS #Stool cultures for C.diff, Ova, and parasites to r/o infectious diarrhea #Fecal leukocytes -WBCs can appear in UC, ischemic colitis, or infectious diarrhea #Colonoscopy to asses the extent of dz and the presence of any complications COMPLICATIONS #IDA #Hemorrhage #Electrolyte disturbances and dehyrdation secondary to diarrhea #Strictures benign and malignant #Colon CA #Sclerosing cholangitis #Cholangiocarcinoma #Toxic megacolon #Growth retardation #Narcotic abuse #Psychosocial issues (e.g. depression) due to chronicity and often disabling nature of the disease
Crohn's Disease
GENERAL CHARACTERISTICS #Chronic transmural inflammatory disease that can affect any part of the GI tract (mouth to anus) but most commonly involves the small bowel (terminal ileum) #Distribution: three major patterns of disease -40% in terminal ileum and cecum -30% confined to SI -25% confined to colon -Rarely other parts of GI tract may be involved (stomach, mouth, esophagus) #Pathology -terminal ileum is the hallmark location -skip lesions -fistulae -luminal structures -noncaseating granulomas -transmural thickening and inflammation-narrowing of lumen -Mesenteric "fat creeping" onto the antiemesenteric border of the small bowel CLINICAL FEATURES #Diarrhea (usually without blood) #Malabsorption and weight loss (common) #Abdominal pain (usually RLQ), nausea, and vomiting #fever, malaise #Extraintestinal manifestations in 15% to 20% of cases (uveitis, arthritis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, aphthous oral ulcers, cholelithiasis, and nephrolithiasis) DIAGNOSIS #Endoscopy (sigmoidoscopy or colonoscopy) with biopsy: typical findings are apthous ulcers, cobblestone appearance, pseudopolyps, patchy (skip) lesions #Barium enema #Upper GI with small bowel follow through COMPLICATIONS #Fistulae #Anorectal disease: fissures, abscesses, perianal fistulas #SBO #Malignancy #Malapsorption of Vitamin B12 and bile acids #Cholelithiasis #Nephrolithiasis-incrased absorption of dietary oxalate can lead to calcium oxalate kidney stones #Aphthous ulcers of lips, gingiva, and buccal mucosa (common) #Toxic megacolon-less common in Crohn's than UC #Growth retardation #Narcotic abuse, psychosocial issues due to chronicity
Acute Pancreatitis
GENERAL CHARACTERISTICS #Inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion #Most patients with acute pancreatitis have mild to moderate disease, but up to 25% have severe disease. There are two forms of acute pancreatitis, mild and severe: -Mild acute pancreatitis is most common and responds well to supportive treatment -Sever acute pancreatitis (necrotizing pancreatitis) has significant morbidity and mortality CAUSES #Gallstones (40%) #Alcohol abuse (30%) #Post-ERCP--pancreatitis #Viral infection #Drugs-sulfonamides, thiazide diuretics, furosemide, estrogens, HIV medications, and many other drugs #Postoperative complications (high mortality rate) #Autoimmune pancreatitis #scorpion bites #pancreas divisium #pancreatic cancer #hypertriglyceridemia, hypercalcemia, hyperparathyroidism #Uremia #Blunt abdominal trauma CLINICAL FEATURES #Symptoms -Abdominal pain, usually in the epigastric region: may radiate to the back; often steady, dull, and severe; worse when supine and after meals -N/V -Anorexia #Signs -low-grade fever, tachycardia, hypotension, leukocytosis -epigastric tenderness, abdominal distension -decreased or absent bowel sounds indicate partial ileus -The following signs are seen with hemorrhagic pancreatitis as blood tracks along the fascial planes *Grey turner sign (flank ecchymosis) *Cullen sign (periumbilical ecchymoses) *Fox sign (ecchymosis of inguinal ligament) DIAGNOSIS #Must fulfill 2/3 criteria: classical clinical presentation (epigastric pain that radiates to back), lab findings, and imaging findings #Laboratory studies -serum lipase and amylase, lipase is more specific -LFTs-to identify the cause (gallstone pancreatitis) -Hypertriglyceridemia, hypoxemia, and leukocytosis may also be present -Order the following for assessment of prognosis (Ranson criteria): Glucose, calcium, hematocrit, BUN, arterial blood gas (PaO2, base deficit), LDH, AST, WBC count #Abdominal Radiograph -limited role -helpful to r/o perf, calcifications suggest chronic -Sentinel loop (area of air filled bowel usually in LUQ, which is a sign of localized ileus) or a colon cut-off sign (air filled segment of transverse colon abruptly ending or "cutting off" at the region of pancreatic inflammation) #Abdominal US -can help in identifying cause of pancreatitis (e.g. gallstones) -useful for following up pseudocysts or abscesses #CT scan of the abdomen -most accurate for diagnosis of acute pancreatitis and identifying complications -indicated in patients with severe acute pancreatitis #Indications for ERCP -severe gallstone pancreatitis w/ biliary obstruction -to identify uncommon causes of acute pancreatitis if dz is recurrent
Mallory Weiss Syndrome
GENERAL CHARACTERISTICS #Mucosal tear at (or just below) the GEJ as a result of forceful vomiting or retching. Usually occurs after repeated episodes of vomiting, but it may also occur after just one episode #MC associated w/ binge drinking in alcoholics, but can be from any d/o that causes vomiting CLINICAL FEATURES #Hematemesis is always present-varies from streaks of blood in vomitus to massive bright red blood DIAGNOSIS #Upper endoscopy
Esophageal Cancer
GENERAL CHARACTERISTICS #There are two pathologic types. In the past SCC accounted for up to 90% of cases. However, the incidence of adenocarcinoma has increased dramatically in the US and it now accounts for up to 50% of new cases #SCC -higher in AA men -MC in upper and midthoracic esophagus -RF include alcohol and tobacco use, diet (nitrosamines, betel nuts, chronic ingestion of hot foods and beverages such as tea), HPV, achalasia, Plummer-Vinson syndrome, caustic ingestion, and nasopharyngeal carcinoma #Adenocarcinoma -more common in caucasians and men (5:1 over women) -MC in distal third of the esophagus/gastroesophageal junction (in 80% of cases) -risk factors: GERD and Barrett's, alcohol, and tobacco #Prognosis is poor: 5 year survival rate is about 30% to 40% if locoregional dz, but only 5% distant metastasis present at diagnosis #Staging -stage I: tumor invades lamina propria or submucosa; nodes negative -stage IV: distant metastasis CLINICAL FEATURES -Dysphagia-MC sx (initially solids only, then progression to liquids) -Wt loss-second most common symptom -Anorexia -Odynophagia-a late finding that suggests extraesophageal involvement (mediastinal invasion) -Hematemesis, hoarseness of voice (recurrent laryngeal nerve involvement) -Aspiration PNA, respiratory sx due to involvement of tracheobronchial tree -Tracheoesophageal or bronchoesophageal fistula -Chest pain DIAGNOSIS -Barium swallow is useful in evaluation of dysphagia. A presumptive dx can be made -Upper endoscopy w/ Bx and brush cytology is required for definitive dx. It confirms the dx in 95% of cases -Transesophageal US helps determine the depth of penetration of the tumor and is the most reliable test for staging local cancer -Full metastatic work-up (e.g. CT scan of the chest/abdomen, CXR, bone scan)
Diverticulosis
GENERAL CHARACTERISTICS #caused by increased intraluminal pressure-inner layer of colon bulges through the focal area of weakness in the colon wall (usually an area of blood vessel penetration) #risk factors: low fiber diets (constipation), positive family history #prevalence increases with age #the most common location is the sigmoid colon. However, diverticula may occur anywhere else in the colon CLINICAL FEATURES #usually asymptomatic and discovered incidentally on imaging (e.g. CT abd/pelvis) or when a complication occurs #vague LLQ discomfort, bloating, constipation/diarrhea may be present #only 10-20% become symptomatic (i.e. develop complications--see below) DIAGNOSIS #Barium enema is the test of choice #abdominal XRs are usually normal and are not dx COMPLICATIONS #Painless rectal bleeding in (up to 40% of patients) -usually clinically insignificant and stops spontaneously -can be severe in about 5% of patients. Colonoscopy may be performed to locate the site of bleeding (mesenteric angiography in certain cases). If bleeding is persistent and/or recurrent, surgery (segmental colectomy) may be needed #________-litis -occurs when feces become impacted in the diverticulum, leading to erosion and micro perforation -can be complicated or uncomplicated. .Uncomplicated accounts for most cases: w/o bowel obstruction, abscess, and fistulas
Hepatocellular Carcinoma (Malignant Hepatoma)
GENERAL CHARACTERISTICS #more than 80% of primary liver cancers and, although rare in the US, accounts for most deaths due to cancers worldwide. High-risk areas include Africa and Asia #there are two pathologic types 1. Nonfibrolamellar (MC): -usually associated with hepatitis B or C and cirrhosis -usually unresectable with very shor survival time (months) 2. Fibrolamellar -usually not associated with hep B or C or cirrhosis -more often resectable: relatively longer survival time -seen most commonly in adolescents and young adults RISK FACTORS -Cirrhosis in association with alcohol or hepatitis B or C (10% of cirrhotic patients) -chemical carcinogens; for example aflatoxin, vinyl chloride, thorotrast -AAT deficiency -Hemochromatosis, Wilson disease -Schistosomiasis -Hepatic adenoma (10% risk of malignant transformation) -Cigarette smoking -Glycogen storage disease (type 1) CLINICAL FEATURES -abdominal pain (painful hepatomegaly) -weight loss, anorexia, fatigue -S/S of chronic liver disease--portal hTN, ascites, jaundice, splenomegaly -paraneoplastic syndromes: erythrocytosis, thrombocytosis, hypercalcemia, carcinoid syndrome, hypertrophic pulmonary osteodystrophy, hypoglycemia, high cholesterol DIAGNOSIS -liver biopsy--required for definitive diagnosis -laboratory tests-hepatitis B and C serology, liver function tests (LFTs), coagulation tests -imaging studies-US, CT scan (chest, abdomen, pelvis); MRI or MRA if surgery is an option (provides more detail about the anatomy of the tumor) -tumor marker elevation (AFP) is useful as a screening tool. AFP level may be elevated in 40% to 70% of patients with HCC, and also is helpful in monitoring response to therapy
Irritable Bowel Syndrome (IBS)
GENERAL CHARACTERISTICS -Idiopathic d/o associated w/ an intrinsic bowel motility dysfunction -commonly associated with depression, anxiety, and somatization. Psych symptoms often precede bowel symptoms. Symptoms are exacerbated by stress and irritants in the intestinal lumen -lab tests are normal, no mucosal lesions on sigmoidoscopy -overall bengin -Sx>3 months CLINICAL FEATURES: #change in frequency/consistency of stool-diarrhea, constipation (or alternating diarrhea and constipation) #cramping abd pain (relieved by defacation)-location varies widely, but sigmoid colon is the common location of pain -bloating or feeling of abdominal distension DIAGNOSIS #Clinical and dx of exclusion #Rome III diagnostic criteria: recurrent abdominal pain/ discomfort >3 days per month in the last 3 months and >2 of the following -pain/discomfort improves w/ defacation -Sx onset is associated with a change in frequency of the stool -Sx onset is associated with a change in the form of the stool #Initial tests that may help exclude other causes include CBC, renal panel, fecal occult blood test, stool examination for ova and parasites, erythrocyte sedimentation rate an possibly a flexible sigmoidoscopy. Order these tests only if there is suspicion of other causes for the symptoms
General Characteristics of Viral Hepatitis
GENERAL CHARACTERISTICS: #Means inflammation of the liver. There are many noninfectious types such as alcoholic, drug-induced, autoimmune, and numerous hereditary diseases that can cause it #Viral causes -five well understood main categories of viral hepatitis: Hepatitis A, B, C, D, and E. Hepatitis viruses are often abbreviated by their type -other viruses that can cause one form or another of hepatitis are EBV, CMV, and HSV. These are not commonly associated with hepatitis in immunocompromised patients #Transmission varies depending on the specific virus -Hepatitis A and E are transmitted via the fecal-oral route and are more prevalent in developing countries -Hepatitis E is particularly prevalent in india, pakistan southeast asia, and parts of africa -Hepatitis B is transmitted parenterally or sexually. Perinatal transmission is also possible and is a significant health issue in parts of africa and asia -Hepatitis D requires the outer envelope of the hepatitis B surface antigen (HBsAG) for replication and therefore can be transmitted only as a coinfection with HBV, or as a superinfection in a chronic HBV carrier -The main route of transmission for hepatitis C is parenteral, and it is therefore more prevalent in IV drug uses. Sexual and perinatal transmission is not common -Hepatitis B, C, and D are the types that can progress to chronic disease
Vitamin K deficiency
GENERAL CHARACTERISTICS: #Obtained through dietary sources and synthesis by intestinal flora #Causes include -Broad spectrum abx-due to suppression of gut flora -Inadequate dairy intake -Total parenteral nutrition (TPN)-unless its added -Malabsorption of Fat soluble vitamins (e.g. small bowel disease, inflammatory bowel disease, obstructive jaundice) CLINICAL FEATURES -petechiae -purpura -easy bruising -gingival bleeding -melena -hematuria DIAGNOSIS -prolonged PT-first laboratory finding due to the short half-life of factor VII -prolonged PTT-follows as other coagulation factors diminish
Small Bowel Obstruction
GENERAL CHARACTERISTICS: #Partial versus complete #Closed loop versus open loop #Proximal versus distal #Dehydration is a key event: Distension-->vomiting-->increased intestinal secretion, decreased absorption-->hypochloremia, hypokalemia, metabolic alkalosis #Hypovolemia-->tachycardia, hypotension, tachypnea, altered mental status, and oliguria CAUSES #Adhesions #Incacerated hernias #Malignancy, intussusception, Crohn's dz, carcinomatosis, superior mesenteric artery syndrome CLINICAL FEATURES #Cramping abdominal pain--if pain is continuous and severe, strangulation may be present #Nausea, vomiting--may be feculent #Obstipation (absence of stool and flatus) #Abdominal distension DIAGNOSIS #Abdominal plain films-dilated loops of small bowel, air-filled fluid levels proximal to point of obstruction, and minimal gas in colon #Barium enema-to identify site of obstruction and r/o LBO
Colorectal Cancer
GENERAL CHARACTERISTICS: #Third most common CA in the US in men and women #Liver is the most common site of distant spread' RISK FACTORS: #Age>50 #Adenomatous polyps (Villous>Tubular) #Personal history of prior CRC #IBD #Family History #Dietary Factors (high fat, low fiber) #Major polyposis syndromes -Familial adnenomatous polyposis (FAP)=lots of polyps -Gardner syndrome=polyps+ostesomas+dental abn+benign soft tissue tumors+desmoid tumors+sebaceous cysts -Turcot syndrome=polyps+cerebellar medulloblastoma or GBM -Peutz-Jeghers=single or multiple hamartomas scattered through GI tract -Familial Juvenile Polyposis Coli=childhood, small risk of CRC, 10-100s of juvenile polyps -Hereditary Nonpolyposis CRC=w/out adenomatous polyposis: Lynch syndrome I=early onset CRC; Lynch syndrome II: female genital tract, skin, stomach, pancreas, brain, breast, biliary tract CLINICAL FEATURES #Hematochezia #Abdominal pain #Change in bowel habits #Unexplained IDA #DIAGNOSIS -Colonoscopy -Biopsy
Gastric Cancer
GENERAL CHARACTERISTICS: -Majority are adenocarcinomas -Gastric cancer is rare in the US -Morphology: Ulcerative (through all layers), Polypoid (solid mass projects into stomach lumen), Superficial spreading (most favorable prognosis), Linitis plastica-"leather bottle"--infiltrates early through all layers, stomach wall is thick and rigid, poor prognosis RISK FACTORS #Sever atrophic gastritis, intestinal metaplasia, gastric dysplasia #adenomatous gastric polyps, chornic atrophic gastritis #Postantrecotmy #Pernicious anemia #Menetrier dz #High intake of preserved foods #Blood type A CLNICAL FEATURES #abd pain and unexplained weight loss are most common symptoms #reduced appetite, anorexia, dyspepsia, early satiety #N/V, anemia, melena , guaiac positive stool DIAGNOSIS #Endoscopy with multiple biopsies--most accurate test #Barium upper GI series--less accurate, but can complement upper endoscopy/biopsy findings #Abdominal CT scan--for staging and to detect presence of METs #FOBT
Cholecystitis
General Characteristics: #obstruction of the cystic duct (not infection) induces acute inflammation of the gallbladder wall #chronic cholecystitis may develop with recurrent bouts of acute cholecystitis #ten percent of patients with gallstones develop acute cholecystitis Clinical features: #Symptoms -always RUQ/epigastric pain; may radiate to the R shoulder or scapula -N/V, anorexia #Signs -RUQ tenderness, rebound tenderness in RUQ -Murphy sign is pathognomonic—inspiratory arrest during deep palpation of the RUQ; not present in many cases -Hypoactive bowel sounds -low grade fever, leukocytosis Diagnosis: #RUQ US is test of choice -high sensitivity and specificity -thickened GB wall, pericholecystic fluid, distended GB wall, and presence of stones #CT scan is as accurate as US but more sensitive inidentifying complications (perforation, abscess, pancreatitis) #Radionucleotide scan (hepatoiminodiacetic acid [HIDA]) -used when US is inconclusive -if no, then acute cholecystitis can r/o -If GB is not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed
HEPATITIS A #Hepatitis A antibody (anti-HAV) #anti-HAV is detectable during acute infection and persists for life, so its presence does not distinguish between active disease and immunity. IgM-specific antibody denotes acute infection HEPATITIS B #HBsAg -present in acute or chronic infection -detectable as early as 1 to 2 weeks after infection -it persists in chronic hepatitis regardless of whether symptoms are present. If virus is cleared, then HBsAg is undetectable #Heptatitis B e antigen (HBeAg) -reflects active viral replication, and presence indicates infectivity -appears shortly after HBsAg #Anti-HBsAg antibody (anti-HBs) -present after vaccination or after clearance of HBsAg--usually detectable 1 to 3 months after infection -in most cases, presence of anti-HBs indicates immunity to HBV #Hepatitis B core antibody (anti-HBc) -assay of IgM and IgG combined -useful bc it may be the only serologic marker of HBV infection during the "window period" in which HBsAg is disappearing and anti-HBsAg is not yet detectable -does not distinguish between acute and chronic infection, and presence does not indicate immunity #Viral load -HBV DNA measured by PCR, if it persists for more than 6 weeks, patient is likely to develop chronic disease HEPATITIS C #Hepatitis C antibody -key marker of HCV infection -sometimes not detectable until months after infection, so its absence does not r/o infection #Viral load: HCV RNA measured by PCR -detectable 1 to 2 weeks after infection--more sensitive than HCV antibody HEPATITIS D #Hepatitis D antibody (anti-HDV) -presence indicates HDV superinfection -the antibody may not be present in acute illness, so repeat testing may be necessary
Hepatitis Serologies
Acute Mesenteric Ischemia
INTRODUCTION #results from compromised blood supply, usually to the superior mesenteric vessels #there are 4 types (three arterial, one venous) a. Arterial embolism (50% of cases): almost all are of cardiac origin (e.g., a-fib, MI, valvular dz) -symptoms are more sudden and painful than other causes b. Arterial thrombosis (25% of cases) -most have atherosclerotic dz -acute occlusion occurs over pre-existing atherosclerotic dz -collateral circulation has usually developed -symptoms are more gradual and less severe than embolic causes c. Nonocclusive mesenteric ischemia (20% of cases) -splanchnic vasoconstriction secondary to low cardiac output -typically seen in critically ill elderly patients d. Venous thrombosis (<10% of cases). Many predisposing factors--infection, hypercoagulable states, oral contraceptives, portal HTN, malignancy, pancreatitis -symptoms may be present for several days or even weeks w/out gradual worsening #The overall mortality rate for all types is about 60% to 70%. If bowel infarction has occurred, the mortality rate can exceed 90% CLINICAL FEATURES #Severe abdominal pain disproportionate to physical findings. pain is due to ischemia and possibly infarction of intestines #Abdominal exam may appear benign even when there is severe ischemia. This can lead to a delay in diagnosis #the acuteness and the severity of pain vary depending on the type #Anorexia, vomiting #GI bleeding (mild) #Peritonitis, sepsis, and shock may be present in advanced disease DIAGNOSIS #mesenteric angiography is the definitive diagnostic test #obtain a plain film of the abd to exclude other causes of abdominal pain #"Thumbprinting" can be seen on barium enema due to thickened edematous mucosal folds
#Instruct pt on adaptive measures: chew food to consistency of pea soup before swallowing; sleep with trunk elevated: avoid eating before sleep #Medical therapy -antimuscarinic agents (dicyclomine)-usually unsatisfactory -sublingual nitroglycerin, long-acting nitrates, and calcium channel blockers *may improve swallowing in early stages of achalasia (b4 esophageal dilation occurs) *most useful in short-term tx (b4 definitive therapy) #Injection of botulinum toxin into the LES during endoscopy -blocks cholinergic activity in the LES -can be effective in up to 65% of cases; however, repeat procedures need to be performed every 2 years #Forceful dilation-mechanical, pneumatic, or hydrostatic -pneumatic balloon dilatation is most effective -lowers basal LES tone by disrupting the muscular ring -can be effective, but there is a 5% risk of perforation #Surgical -"Heller myotomy"-circular muscle layer of LES is incised -usually reserved for patients who do not respond to dilation therapy #Early results are promising (80% to 90% of patients experience good to excellent palliation of dysphagia at 1 year) #Long-term data are needed
Treatment of Achalasia
#Supportive measures -IVF -Broad spec abx #Direct intra-arterial infusion of papaverine (vasodilator) into the superior mesenteric system during arteriography is the therapy of choice for all arterial causes of acute mesenteric ischemia. Relieves occlusion and vasospasm #Direct intra-arterial infusion of thrombolytics or embolectomy may be indicated in some patients with embolic acute mesenteric ischemia #Heparin anticoagulation is the treatment of choice for venous thrombosis #Surgery (resection of nonviable bowel) may be needed in all types of acute mesenteric ischemia if signs of peritonitis develop
Treatment of Acute Mesenteric Ischemia
#Patients with mild acute pancreatitis -NPO -IV fluids: LR (balanced crystalloids) > Nl saline (concern for hyperchloremic metabolic acidosis) -Pain control: Fentanyl and Meperidine>Morphine (can increase sphincter of oddi pressure) -NG tube if severe N/V or ileus present -All pt with gallstone pancreatitis should have cholecystectomy after recovery from pancreatitis. These pt may benefit from early ERCP #Patients with severe pancreatitis -Admit to the ICU -Early enteral nutrition in the first 72 hours is recommend through NJ tube -If severe acute pancreatitis has not resolved in a few days, supplemental parenteral nutrition should be started -If more than 30% of the pancreas is necrosed, prophylactic abx (imipenim) should be considered to prevent infection (which has high morbidity and mortality)
Treatment of Acute Pancreatitis
Most cases do not require treatment. Consider resection if the patient is symptomatic or if there is a high risk of rupture (as with large tumors)
Treatment of Cavernous Hemangiomas
#Admission -hydration w/ IV fluids -bowel rest (NPO) -IV abx -analgesics -correction of electrolyte abnormalities #Surgery-cholecystectomy -Early (w/in first 24 to 48 hours) -recurrence rate with nonsurgical tx is as high as 70% -in most patients, early cholecystectomy is preferred #In critically ill with high surgical risk, percutaneous cholecystectomy tube placement for drainage of the gallbladder is an alternative to immediate surgery
Treatment of Cholecystitis
#No tx if the patient is asymptomatic #Elective cholecystectomy for patients with recurrent bouts of biliary colic
Treatment of Cholelithiasis
#Treat underlying cause--for example, abstinence from alcohol, interferons for hepatitis B and C #Avoid agents that may cause injury to liver, such as acetaminophen and alcohol #Once it develops, aim treatment at managing any complications that arise, as described above. The most serious complications are variceal bleeding, ascites, and hepatic encephalopathy #Liver transplantation is the only hope for a cure. Abstinence from alcohol for more than 6 months is required before a patient is eligible for transplantation. decision to proceed to liver transplantation depends on quality of life, severity of disease, and absence of contraindications
Treatment of Cirrhosis
#Surgery is the only curative treatment. Surgical resection of tumor-containing bowel as well as resection of regional lymphatics #CEA level should be obtained before surgery #Utility of adjuvant therapy (chemo or radiation) depends on the stage of tumor #F/u is important -stool guaiac test -annual CT scan of abd/pelvis and CXR for up to 5 years -colonoscopy at 1 year and then every 3 years -CEA levels every 3 to 6 months: recurrence, very high=liver involvement -about 90% of recurrence is w/in 3 years after surgery
Treatment of Colorectal Cancer
#Uncomplicated -IV antibiotics -Bowel rest (NPO) -IV fluilds *Mild episodes can be treated on outpatient basis if pt is reliable and has few or no comorbid conditions. #If sx persist after 3 to 4 days, surgery, resection of the involved segment, may be necessary. #Abx continued for 7 to 10 days. After successful tx, about one third has recurrence-->surgery recommended for recurrent episodes #Complicated diverticulitis-surgery indicated
Treatment of Diverticulitis
#Palliation is the goal in most patients bc the dz is usually advanced at presentation #Surgery (esophagectomy) may be curative for pt w/ dz in stage 0, 1, or 2A # Chemotherapy plus radiation b4 surgery has been shown to prolong survival more than surgery alone
Treatment of Esophageal Cancer
#Surgical resection with wide (>5cm) margins (total or subtotal gastrectomy) with extended lymph node dissection #Chemotherapy may be appropriate in some cases
Treatment of Gastric Cancer
#Liver resection (in the 10% of patients who have resectable tumors) #LIver transplantation if diagnosis is made early #If unresectable, consider transcatheter arterial chemoembolization (TACE), radiofrequency ablation, or selective internal radiation therapy
Treatment of Hepatocellular Carcinoma (Malignant Neoplasm)
#For mild Sx, diet and lifestyle changes (e.g. avoiding dairy products, excess caffeine). Manage the Sx below as indicated -Diarrhea: diphenoxylate, loperamide -Constipation: colace, psyllium, ciapride -Abdominal pain: antispasmodics (e.g. pinaverium, trimebutine, peppermint oil, cimetropium/dicylomine), antidepressants, rifaximin
Treatment of Irritable Bowel Syndrome
#90% of cases stop bleeding without any treatment #Treatment is surgery -(oversewing the tear) -Or angiographic embolization if bleeding continues, but this is rarely necessary. #Acid suppression is used to promote healing
Treatment of Mallory Weiss Syndrome
#Active (vaccine) and passive (immunoglobulin) immunization are available for both hepatitis A and B. It is the standard of care for infants and healthcare workers to be vaccinated for HBV #Travelers often receive vaccinations for HAV. Passive immunization can be given for people who are exposed to this virus #Treatment for hepatitis A and E is supportive #Chronic HBV--treatment is indicated if high viral load or ALT elevation. Treat with nucleotide/nucleoside analogs (tenofovir, entecavir). Alternatively, tx with pegylated-interferon (peg-IFN) #Chronic HCV--tx with antiviral agents -interferon-free regimens: current standard of care with newer direct-acting antiviral agents (e.g. ledipasvir, sofosbuvir, simeprevir, and many others) can cure chronic HCV. Very expensive. Tx regimen depends on stage of liver fibrosis, tx history ,and HCV genotype -interferon-containing regimens: peginterferon and ribavirin. Associated with a high frequency of side effects, such as hematologic toxicity (neutropenia, thrombocytopenia, anemia), fatigue, flu-like symptoms, and neuropsychiatric symptoms #Consider liver transplantation in advanced disease, although recurrence can occur after transplantation. Hepatitis C is the most frequent indication for liver transplantation in the United States
Treatment of Viral Hepatitis
#Vitamin K replacement (oral or subcutaneous)-may take several days for PT to return to normal #FFP if bleeding is sever and emergency treatment is necessary
Treatment of Vitamin K deficiency
#Appendectomy (usually laparoscopic): up to 20% of patients who are diagnosed with acute appendicitis are found to have a normal appendix during surgery. Bc the illness is potentially life threatening, this is an acceptable risk even during pregnancy #Low-risk pt may be considered for medical management alone with abx to avoid surgery. Close f/u is necessary in case urgent surgery is required
Treatment of appendicitis
#Diet and behavioral modification are the most important aspects of treatment. Advise the pt to -increase physical activity -eat high-fiber foods -increase fluid intake #Bulk laxatives are preferred over osmotic laxatives in patients that do not respond to diet and lifestyle changes #Use an enema, such as a disposable Fleet enema, for temporary relief if no bowel movement occurs despite the above measures or if the patient is bedridden #If obstruction is present, urgent surgery consultation is indicated
Treatment of constipation
discontinue oral contraceptives; surgically resect tumors >5cm that do not regress after stopping oral contraceptives (otherwise there is a risk of rupture)
Treatment of hepatocellular adenoma
#Medical -Systemic corticosteroids (prednisone): initial therapy for low risk patients with diffuse dz or L sided colon dz-if unable to taper consider IS or biologic -Budesonide: used in low risk patients with mild dz in ileum or righ colon, if unable to taper consider IS or biologic -Biologic agent (TNF inhibitor) can be used as monotherapy or in combo with thipurine (azathioprine or 6-mercaptopurine) or methotrexate in pt with moderate to severe disease #Surgery (eventually required in most patients) -Reserved for complications of Crohn's disease or for those who have persistent symptoms despite best medical management -involves segmental resection of involved bowel -Dz recurrence after surgery is high. Up to 50% of patients experience dz recurrence at 10 years postoperatively -Indications for surgery include SBO, fistulae, disabling dz, and perforation or abscess #Nutritional supplementation and support--parenteral nutrition is sometimes necessary
Treatment of inflammatory bowel disease