GASTROINTESTINAL SYSTEM/NUTRITION-2012 Dipali Yeh M.S., PA-C University of Medicine and Dentistry of New Jersey

ESOPHAGUS  ESOPHAGITIS Infectious esophagitis General Considerations Rare, except in immunocompromised Risks Aids Leukemia/Lymphoma Solid organ transplant Uncontrolled DM Chronic systemic steroid use Causes Fungal-Candida Viral-HSV, CMV

Clinical Features Odynophagia (painful swallowing) Dysphagia (difficulty swallowing) substernal chest pain involvement of colon/retina-CMV herpes labialis-HSV Diagnosis Endoscopy Large/deep ulcers-CMV/HIV Multiple shallow ulcers-HSV White plaques-Candida

Treatment Etiology Initial treatment Refractory Candida Fluconazole/ketoconazole Itraconazole/amphotericin HSV Acyclovir Foscarnet CMV Gancyclovir Foscarnet (neutropenia) (Renal failure, ↓Ca+, ↓Mg+)

Pill-induced esophagitis General Considerations Offending agents: NSAIDs, KCl, antibiotics, iron Risks Swallowed without water Supine Hospitalized/bed-bound patients Clinical Features Odynophagia/Dysphagia Retrosternal chest pain Diagnosis Endoscopy-deep/shallow ulcers can treat empirically Treatment Prevention: 4oz water, remain upright x 30 min Reflux esophagitis-covered in GERD

 MOTILITY DISORDERS General Considerations Factors involved Neurological Intrinsic/external blockage Peristalsis malfunction Distal Esophagus=more susceptible Types Achalasia Scleroderma Esophageal spasms Zenker’s diverticulum-mechanical disorder

Achalasia General considerations Usually b/w 30-60yrs old Idiopathic LES ↑, peristalsis ↓ Clinical features gradual, progressive dysphagia > solids + liquids adopt compensatory maneuvers regurgitation (+)weight loss Diagnosis Barium swallow: “parrot beak” appearance Treatment Botox injection Pneumatic dilatation Surgical myotomy

Scleroderma General considerations Most common GI organ affected CREST syndrome Clinical features “Heartburn” 20% develop Barrett’s esophagus Diagnosis Barium swallow: aperistalsis Manometry: ↓LES sphincter Treatment Cornerstone: PPI-omeprazole (Prilosec) Lifestyle modifications- small, frequent meals & avoid nighttime meals

Esophageal Spasms General considerations ? deficiency of NO in esophageal body Clinical features Dysphagia/intermittent chest pain May/may not be associated with eating Diagnosis

Barium swallow: “corkscrew” esophagus Manometry: (+)contractions/(-)progression Treatment Empirically, smooth muscle relaxants Hycosamine, Ca+-channel antagonists (nifedipine), nitroglycerin Anti-depressants>low-dose tricyclics Imipramine (Tofranil)

Zenker’s Diverticulum General considerations Outpouching posterior hypopharynx Older patients/insidious onsent Clinical features Halitosis Regurgitate undigested food several hrs postprandially Diagnosis Barium radiograph Treatment Asymptomatic=no treatment Surgery-myotomy/diverticulectomy Complications Aspiration/bronchiectasis/lung abscess

 MALLORY-WEISS TEAR General Considerations Tear in gastroesophageal junction Secondary to forceful vomiting/retching Associated with etoh abuse Clinical features-hematemesis Diagnosis-endoscopy Treatment Most heal spontaneously w/in 48 hours Endoscopic epinephrine/thermal coagulation

 ESOPHAGEAL NEOPLASMS General Considerations 50-70 yrs old M:F=3:1 Two types Squamous cell carcinoma: 95% Adenocarcinoma Mets>mediastinum (esophagus has no serosa) Risk factors Squamous cell: smoking/ETOH abuse Adenocarcinoma: obesity, Barrett’s esophagus

Clinical features Progressive dysphagia>solid food + weight loss Pneumonia/voice hoarseness Lymphadenopathy/hepatomegali=mets Diagnosis Initial-biphasic barium study Confirm-biopsy Treatment Surgical-esophagectomy Radiation/adjunct chemo Prognosis 5yr survival rate: <20%

 ESOPHAGEAL STRICTURES General Considerations Complication of esophagitis Clinical presentation Resolution of heartburn Progressive sold food dyphagia-months>years Diagnosis Biopsy-r/o etiol from cancer Treatment Endoscopic dilation Long term PPI Refractory: endoscopic triamcinolone injection

 ESOPHAGEAL VARICES General Consideration Develop secondary to portal hypertension Most common cause of GIB secondary to portal HTN Found in 50% of patients with cirrhosis 30% of patients with varices bleed, but 50% of those will spontaneously cease without treatment Risk factors which increase chance of bleeding Size of varices Presence of red wale markings Severity of liver disease Active alcohol abuse Clinical features: acute GI hemorrhage Diagnosis: Established clinically: patient with cirrhosis presents with hematemesis Treatment Hemodynamic support Pharmacological therapy Vasoactive medications-octreotide to reduce blood flow and portal pressure Vitamin K-cirrhosis patients with abnormal PT; 10mg SQ Lactulose-for encephalopathy Antibiotic prophylaxis-fluoroquinolon/3rd generation cephalosporin Endoscopic support-banding or sclerotherapy Mechanical tamponade with NGT balloon Transvenous intrahepatic portosystemic shunt procedure: reserved for bleeding refractory to treatment Mortality 30% during 1st episode of bleeding 50% within 6 weeks

 STOMACH  GERD/Reflux Esophagitis General Considerations Recurrent reflux of gastric contents into distal esophagus LES relaxed 10% of general population; 50% infants have reflux Clinical Features Heartburn-most common

Hoarseness Halitosis Cough Atypical chest pain Diagnosis Clinical based on history Endoscopy for alarm symptoms: Refractory heartburn Dysphagia Weight loss GI bleed/anemia 45+ years old w/ new onset symptoms Treatment #1: appropriate lifestyle modification Weight loss due to ↑ association with obesity PPI’s: superior to H2 blockers; 4weeks empirically -for short term relief & long-term tx -most powerful anti-GERD medication -first-line treatment Omeprazole (Prilosec) 20mg/d Lansoprazole (Prevacid) 30mg/d Pantoprazole (Protonix) 40mg/d

HEARTBURN/ACID REFLUX ↓ (+)Alarm Symptoms (-) Alarm Symptoms ↓ ↓ Immediate endoscopy Lifestyle changes ↓ ↓ Successful Not successful ↓ ↓ Continue Trial of PPI’s (superior to H2 blockers)

 GASTRITIS/DUODENITIS General Considerations Histological evidence of inflammation Causes H. pylori NSAID’s Stress Alcohol use Pernicious anemia Clinical features Dyspepsia Abdominal pain Generally reflects underlying etiology Diagnosis Endoscopy with biopsy Presence of H. pylori (urea breath test) Specific tests to r/o etiology (i.e. vitamin B12 & CBC for pernicious anemia) Treatment Remove the causative agent (i.e. NSAIDs, alcohol) Treat the underlying condition

H. PYLORI Gram-negative, spiral shaped bacillus Leads to gastric mucosal inflammation with PMNs and lymphocytes Associated with PUD/Gastric adenocarcinoma Urease-producing agent=detected by Urea breath test Can also do fecal antigen assay/serology Treatment -Triple therapy: PPI/Bismuth + 2 antibiotics -Quadruple therapy: PPI + Bismuth + metronidazole (Flagyl) + tetracycline Or PPI + Bismuth + levofloxacin (Levaquin)+ doxycycline *If symptoms persist, continue antisuppressive therapy when antibiotic therapy is complete

 PEPTIC ULCER DISEASE General Considerations Refers to gastric or duodenal ulcers 80-90% of patients have dyspepsia Most NSAID ulcers are asymptomatic H. pylori is the most common cause of PUD Other causes:NSAIDs, stress, irritant, alcohol M: F is equal Clinical features Hallmark is epigastric pain “gnawing/hungerlike” Duodenal ulcer: improves with food Gastric ulcer: worsens with food/associated with weight loss Diagnosis Endoscopy is definitive/procedure of choice Barium study: 30% false negative rate; less sensitive Urea breath test for H. pylori Treatment Avoid irritating factors: smoking, NSAIDs, alcohol See combination therapy for H. pylori Misoprostol Prostaglandin analog Prophylactic treatment Indications of use: Patients who require daily NSAID use Hx complications (bleeding) Use of chronic steroids/anticoagulants

 GASTRIC NEOPLASMS Predominantly malignant 90-95% are adenocarcinomas Also: Zollinger-Ellison Syndrome (Gastrinoma)

Gastric adenocarcinoma General Considerations Typically occurs between 50-70 yrs old Uncommon in 30yrs and younger M:F=2:1 5-year survival is <20%

Risk Factors Environmental H. pylori infection Diet: excess salt/nitrates, deficient fruits/vegetables Low socioeconomic status Cigarette smoking Genetic Familial history Associated with hereditary nonpolyposis colorectal CA Clinical features Generally asymptomatic until disease is advanced Dyspepsia + weight loss + GI bleed Signs of metastasis: Virchow’s node: L supraclavicular lymph node Sister Mary Joseph Nodule: umbilical nodule Krukenberg tumor: mets to the ovaries Diagnosis Iron deficiency anemia Endoscopy: malignant ulcer: irregular base and irregular folds Treatment Surgery Only chance for cure for 25-30% of patients Medical therapy Somewhat responsive to chemotherapy Radiation alone is ineffective Combination chemo + radiation improves survival from 27 mo to 36 mo vs surgery alone

Gastric Lymphoma General considerations Can be primary or mets from elsewhere by lymph spread 95% are non-Hodgkin B cell lymphoma Risk factor: H. pylori infection increased by 6-fold Clinical presentation Same as adenocarcinoma Dyspepsia, weight loss or anemia Diagnosis Endoscopic biopsy Findings: thickened folds, mass, ulcer

Treatment Depends on staging With or without radiation or chemo

ZES (Gastrinoma) General considerations Gastrin-secreting tumor Consider this diagnosis in patients with refractory PUD Only 1% of PUD cases are caused by ZES Most common locations: duodenum/pancreas 1/3 associated with MEN-1 Clinical manifestations PUD symptoms refractory to treatment Hearburn 20% Secretory diarrhea 60-70% Diagnosis Fasting serum gastrin level > 150pg/ml (normal: 100pg/ml) pH < 2.0 Imaging: SRS w/ SPECT somatostatin-receptor scintigraphy w/ single photon emission CT CT/MRI for metastatic disease Treatment Control hypersecretion: oral PPI’s Goal: achieve acid output of <10meq/h. Most important predictor of survival: hepatic mets 30% of patients with hepatic mets=10yr survival rate Surgical resection of gastrinoma before hepatic spread=curative 15-year survival of patients w/o hepatic spread at dx=95%

 PYLORIC STENOSIS General considerations Pyloric hypertrophy causes gastric outlet obstruction M:F = 5:1 Clinical features Projectile vomiting which is progressive and nonbilious Child remains hungry Age: 4-6 weeks (+)weight loss (+)dehydration

Physical exam: olive-shaped mass to the R of the umbilicus Diagnosis Ultrasound demonstrates lesion Barium swallow shows “string sign” Treatment Ramsted pyloromyotomy

 GALLBLADDER DISEASE  GALLSTONE DISEASE  CHOLELITHIASIS/ACUTE CHOLECYSITIS General considerations Often asymptomatic Majority: cholesterol stones F>M Risk factors age Obesity Rapid weight loss (i.e. bariatric surgery) DM/Glucose intolerance/insulin resistance Family history Clinical features Nausea, vomiting Bloating RUQ pain, 15-30 minutes postprandially Fever (absent in biliary colic/present in acute cholecystitis) Murphy’s sign (inhibit inspiration) Diagnosis Leukocytosis (absent in biliary colic; >11,000/uL in acute cholecystitis) The following may indicate complication of disease such as pancreatitis: Elevated liver function tests Elevated serum amylase/lipase Elevated serum bilirubin RUQ ultrasound (+)gallstones in biliary colic (+)gallstones +GB wall thickening in acute cholecystitis

HIDA scan Hepatobiliary iminodiacetic acid Most specific test for acute cholecystitis 95% sensitivity ERCP Endoscopic retrograde cholangopancreatography Identify features of biliary obstruction Treatment: acute cholecystitis Medical stabilization IV fluids Bowel rest Antibiotics Ampicillin 2g IV q6hrs Aminoglycoside (gentamycin 5.1 m/k q24hrs) Pain management: morphine or meperidine Surgical Cholecystectomy, generally 2-4 d after admission Gangrene/perforation=immediate cholecystectomy

 CHOLEDOCHOLITHIASIS/CHOLANGITIS General considerations Common bile duct stones which descend from the gallbladder Risk factors Infection Biliary stasis Acutely post-cholecystectomy Choledocholithaisis=most common cause of acute bacterial cholangitis Organisms most likely involved with acute bacterial cholangitis: E.coli Klebsiella Enterococcus Enterobacter Clinical features Charcot triad: RUQ pain, fever, jaundice in 50-70% of cases Reynold’s pentad=Charcot’s triad + AMS + hypotention>>Sepsis Diagnosis/Treatment RUQ sono: good initial test detecting biliary dilation or stones Leukocytosis w/ left shift Increased LFT’s, bilirubin and alkaline phosphatase

Broad spectrum antibiotics ERCP: gold standard for diagnosis and treatment of bile duct stones After successful endoscopic therapy> lap cholecystectomy

Primary Sclerosing Cholangitis General considerations Etiology unknown; thought to be autoimmune Chronic thickening of bile duct wall 80% associated with inflammatory bowel disease, particularly Ulcerative colitis M:F = 7:3 Mean age at diagnosis 39 (range 21-67 years) Clinical features Jaundice/pruritis-most common Hepatomegaly/splenomegaly on exam Diagnosis 90% of patients have elevated alkaline phosphatase Same labs as acute cholangitis Biopsy of the bile duct shows “onion ring” fibrosis Treatment No treatment slows disease progression Liver transplant-only potential curative therapy Survival rate s/p transplant: 83% at 1 year and 73% at 5 years

 LIVER  HEPATITIS General Considerations Described as acute vs chronic Causes Viral-most common Toxins (alcohol, acetaminophen)  ACUTE VIRAL HEPATITIS General Considerations A&E are self-limited and mild with no long-term sequelae B, C & D are transmitted parenterally/mucous membrane contact D is only seen in conjunction with Hep B Hep C & HIV are frequent coinfections Clinical features Fatigue, malaise, anorexia Tea-colored urine Diagnosis Hepatitis A Anti-HAV=immunoglobulin M antibody Can be detected with onset of clinical disease HAV IgG indicates resolved Hep A Hepatitis B Serological markers: HBsAg (Hep B surface antigen) -detected during acute or chronic infection -presence indicates person is actively infectious Anti-HBs (Hep B surface antibody) -indicates recovery and immunity from infection -also indicates person has been successfully vaccinated against Hepatitis B Anti-HBc (Hep B core antibody) -appears at onset of symptoms in acute infection -indicates previous or ongoing infection IgM anti-HBc (IgM antibody to Hep B core antigen) -indicates recent infection within the last 6 months -indicates acute infection

* Hepatitis B antigen. † Antibody to HBeAg. § Antibody to hepatitis B core antigen. ¶ Hepatitis B surface antigen. ** Immunoglobulin M. http://www.cdc.gov/immigrantrefugeehealth/guidelines/domestic/viral- hepatitis-figure4.html

Hepatitis C -Anti-HCV antibodies via enzyme immunoassay -Presence of RNA virus in absence of antibodies= Hepatitis D -anti-HD antibodies, ant-HD IgM & RNA are detectable by PCR -patients who are HBsAG (+)should be tested for Hep D Hepatitis E -anti-HEV IgM antibodies Treatment HAV=self-limited; no specific antiviral treatment HBV -most patients spontaneously clear the infection -lamivudine may reduce need for liver transplant -use standard hygiene/precautions to prevent HDV coinfection HCV -treatment should be considered to reduce chronic infection and viremia -pegylated interferon ά-2a or 2b 180 μg/wk

-ribavirin should be added for patients with slow RNA decrease -Needlestick exposure patients: do not treat with above meds; monitor RNA and LFT’s at baseline, weeks 2, 4 and 6 months s/p exposure. Treat if documented infection Prevention HAV vaccine -travelers to endemic regions -MSM -chronic liver disease -healthcare providers HBV -barrier protection during intercourse for those infected -Vaccination 0, 1, 6 mos of HBsAg HCV -screen blood products -apply standard surgical hygiene -needle exchange programs -NO vaccine exists HEV -improved public hygiene=best defense

 CHRONIC VIRAL HEPATITIS General considerations Defined by chronic infection > 6 months Only applies to HBV, HCV, HDV Chronic HBV/HCV=leading cause of cirrhosis/hepatocellular CA Clinical features Fatigue, nausea, jaundice, anorexia Sleep disorders RUQ pain Diagnosis AST/ALT 2-5 times (ALT>AST) Alkaline phosphatase usually minimally elevated unless (+)cirrhosis Liver biopsy-critical for diagnosis and determine disease severity Treatment Chronic Hep B: not curable; can be controlled with antivirals Chronic Hep C: curable, but less than ½ pts w/ treatment are cured Chronic Hep D: peg IFN-ά 9 million u 3/wk Autoimmune: responds to corticosteroids and azathioprine

 CIRRHOSIS General considerations Irreversible fibrosis & nodular regeneration of liver Main factors: chronic Hep C & alcoholic liver disease Two main complications: portal HTN & liver insufficiency Clinical features Weakness, fatigue, weight loss Nausea, vomiting, anorexia Abdominal pain & hepatomegaly Late-stage disease: esophageal varices, encephalopathy, ascites Diagnosis Leukopenia Anemia Decreased albumin Mild AST elevation Treatment Abstinence from alcohol Ascites: -salt restriction/bed rest/spironolactone 100mg daily -if develop ↑K+, switch to furosemide (Lasix) Varices -non-selective β-blockers (propranolol) to ↓ portal pressures -octreotide -endoscopic therapy Encephalopathy -lactulose 15-30ml twice daily -TIPS procedure Surgical option: Liver transplant

 LIVER NEOPLASMS General considerations Can be malignant or benign Benign include Cavernous hemangioma Hepatocellular adenoma Malignant-may be primary or metastatic Liver is common site of mets from lung and breast CA Primary Hepatocellular CA: Risk factors Hepatitis B Hepatitis C

*Cirrhosis-major predisposing factor Aflatoxin B1 exposure (Aspergillus) Clinical features Anorexia, cachexia, abdominal pain, weight loss (+)bruit/friction rub on auscultation Diagnosis leukocytosis Tumor marker: serum ά-Fetoprotein: > 200ng/ml=95% specificity If history of cirrhosis: surveillance u/s q6mo CT/MRI=diagnostic modalities of choice Needle biopsy not recommended for resectable tumors Treatment Benign: only treat if risk of rupturing hepatic capsule Early stage w/ no liver dysfunction=surgical resection Local tumor ablation Liver transplant Prognosis Surgical resection 5-year survival rate 50-70% Liver transplant w/ early dz at detection 5-yr survival rate 70-80%

 PANCREAS  ACUTE/CHRONIC PANCREATITIS General Considerations Most common causes: Cholelithiasis & alcohol abuse Also: abdominal trauma, hypercalcemia, drugs (6-MP & azathioprine) & toxins (organophosphate insecticides) Clinical features Hallmark: abdominal pain, nausea, vomiting Classic epigastric abdominal pain radiating to the back Fever Tachycardia, hypotension and dyspnea in severe cases Grey-Turner sign: flank ecchymosis Fluid & blood from retroperitoneum Cullen sign: umbilical ecchymosis track into these spaces Diagnosis Elevated serum amylase/lipase Lipase is more sensitive/specific Leukocytosis Elevated LFTs with biliary obstruction

Ranson’s Criteria for Poor Prognosis: AT ADMISSION W/IN 48 HOURS

Age>55yrs ↓ in HCT by >10% Wbc>16,000/μL Estimated fluid sequestration of Glucose>200mg/dl >6L LDH>350IU/L Serum Ca+ < 8 mg/dl AST>250IU/L PaO2 < 60mm Hg BUN ↑ > 5 mg/dL after hydration Base deficit > 4 mmol/L Risk of mortality rises with each additional factor Total score >/= 3: definition of severe pancreatitis Imaging: abdominal ultrasound to evaluate edema/associated fluid collections/pancreatic enlargement CT=more accurate than u/s to confirm diagnosis Treatment: General supportive care Keep NPO Pain control: hydromorphone (Dilaudid) 1-2 mg IV q4-6hrs Fluid resuscitation w/in 24 hours (achieve urine output 0.5ml/kg/hr) Fluids preferred: crystalloid: NS, 1/2NS or LR Nausea/vomiting Promethazine (Phenergan) 25mg IV three times daily Ondansetron (Zofran) 4-8 mg IV q8hours NG suctioning if intractable When do we progress to a solid diet? (+)bowel sounds (+)appetite resolved (+) nausea has resolved (+)enzymes have normalized (+)pain is controlled

CHRONIC PANCREATITIS General considerations 70-80% of cases secondary to alcohol abuse in the US Also: cholelithiasis, PUD, hyperlipidemia ? evidence that cigarette smoking alone as an etiology Classic triad: pancreatic calcification/steatorrhea/DM-only occurs in 20% of patients Clinical features Most common symptoms: abdominal pain

Same as acute + fat malabsorption + steatorrhea Diagnosis Elevated fecal fat due to exocrine pancreatic insufficiency DM due to endocrine insufficiency Pancreatic calcifications on abdominal x-ray in 20-30% of cases Treatment Definitive: treat the underlying cause (i.e. abstinence from alcohol) Analgesics: tramadol (Ultram) 50mg q6hrs Pancreatic enzyme therapy for severe disease Steroids if autoimmune in etiology

 PANCREATIC NEOPLASM General considerations 4th most common cause of cancer death in the US Risk factors Age Tobacco use (causes 25% of cases) Heavy alcohol use Previous abdominal radiation Family history 75% occur in the pancreatic head Clinical features Abdominal pain Diarrhea due to malabsorption Weight loss Courvoisier’s sign: palpable gallbladder-indicates obstruction by neoplasm Diagnosis Anemia Impaired glucose tolerance Steatorrhea CT scan: preferred imaging study Tumor marker: CA-19-9-not sensitive; just for monitoring Treatment If no mets=surgical resection of adenocarcinoma After successful resection, adjuvant chemotherapy If unresectable disease=combination chemo and radiation If metastatic disease is present: manage pain and local complications Prognosis: poor: 5-year survival rate is 2-5%

 SMALL INTESTINE/COLON  APPENDICITIS General Considerations Most common acute surgical emergency involving the abdomen Fecalith found in <30% Patients usually b/w 10-30 years old Clinical features Early periumbilical pain Later: localization of pain to the RLQ (McBurney’s point) Associated symptoms: nausea, vomiting, fever Psoas sign: patient is supine and attempts to raise R leg against resistance Obturator sign: patient is supine and attempts to flex and internally rotate the R hip with the R knee bent Diagnosis Leukocytosis in 80% of cases Imaging diagnostic modality of choice: CT scan Treatment Surgical appendectomy, preferably laproscopically Antibiotics: cefotetan 2g IV or ticarcillin-clavulanate (Timentin) 2gIV In the setting of perforation, ceftriaxone (Rocephin) & metronidazole (Flagyl) once daily x 7-10 days

 CELIAC DISEASE General considerations Inflammatory condition of the small intestine (precise pathogenesis unclear) Precipitating factors: ingestion of wheat, rye and barley Dietary disorder due to immunologic response to gluten High-risk groups 1st degree relatives Type 1 DM Autoimmune thyroid disease Associated with HLQ-DQ2(+) patients Clinical features Typical symptoms: weight loss, chronic diarrhea, abd distention, growth retardation Rash (dermatitis herpetiformis) Diagnosis 2 tests w/ highest accuracy:

IgA endomysial antibody IgA tTG antibody Standard method for confirmation of diagnosis: endoscopic biopsy of the distal duodenum or proximal jejunum Treatment Remove all gluten from the diet 70% of patients have osteopenia/osteoporosis>bone densitometry Vitamin D/calcium supplementation if necessary

 CONSTIPATION General considerations Occurs in 10-15% of adults More common in women First step in evaluation: determine what is meant by “constipation” Most common causes: inadequate fiber/fluid intake & poor bowel habits Primary: slow transit time Secondary: due to systemic disorders/medication side effects Clinical features Primary: infrequent BM’s, abdominal bloating, excess straining Secondary: look for “alarm symptoms” Hematochezia Weight loss Anemia (+)fecal occult blood test Diagnosis: if refractory to treatment, colonic transit studies are warranted Treatment Dietary/lifestyle measures 30g fiber/day (psyllium, methylcellulose) Regular exercise Adequate fluid intake Discontinue medications which may be causing constipation Osmotic laxatives: ↑ H2O secretion into intestinal lumen Magnesium hydroxide Lactulose Polyethylene glycol Stimulant laxatives-stimulate fluid secretion & colonic contractin Bisacodyl Senna Cascara

Complication: FECAL IMPACTION Clinical presentation-decreased appetite, abd pain, distention Firm feces palpable on digital rectal exam Treatment Initial: Saline or mineral oil enema Subsequent: digital disimpaction of fecal material Long-term goal: maintain soft stool & regular bowel movements

 DIVERTICULAR DISEASE General considerations Colonic diverticulosis: uncomplicated herniations of the mucosa/submucosa 50-80% occur in patients >80yrs old Associated with Western population/low dietary fiber More common in sigmoid (highest intraluminal pressures) Asymptomatic/uncomplicated-no imaging needed Recommended to have high fiber diet/fiber supplements Diverticulitis develops in 10-25% of patients Clinical manifestations of diverticulitis Anorexia, LLQ pain, fever LLQ tenderness on PE 5% have diverticular bleeding Diagnosis of diverticulitis Leukocytosis 70-80% Imaging options: CT scan: may show inflammation Barium study: not recommended in the acute setting Due to risk of perforation Colonoscopy: after acute syndrome has resolved and patient is stable Treatment Uncomplicated with mild symptoms: broad spectrum antibiotics Ciprofloxacin (Cipro)/levofloxacin (Levaquin) + metronidazole (Flagyl) x 7-10 days Clear liquid diet & advance as tolerated Unresponsive to outpatient therapy/unable to tolerate PO intake IV antibiotics Hospitalization for hydration Surgical management

Peritonitis Perforation Obstruction Abscess formation: CT-guided drainage & surgery s/p 6 wks Avoid nuts/seeds/popcorn? Recent studies negate this need

 INFLAMMATORY BOWEL DISEASE General considerations Includes ulcerative colitis and crohn’s disease Common in developed countries M=F Peak incidence 15-30 yrs and 2nd peak in 7th decade Risk factor: family history/Ashkenazi Jew descent Cigarette smoking: bad for Crohn’s/Good for UC

Clinical features CROHN’S UC

Smoking Poor prognosis Improved course

Sites of GI Esophagus>anus Colon (rectal involvement (rectal sparing) involvement)

Lesions “Skip lesions” Continuous disease

Transmural (+) (-) involvement

Symptoms RLQ Abd pain/hematochezia pain/diarrhea/fatigue

Surgery Not curative Can be curative

Extraintestinal manifestations of IBD: Skin Pyoderma gangrenosum Erythema nodosum (pretibial) Vasculitis

Eyes Iritis Conjunctivitis Uveitis

Joints Arthritis Ankylosing spondylitis

Liver Sclerosing cholangitis Hepatitis

Diagnosis Colonoscopy: initial preferred endoscopic test for patients with Diarrhea/hematochezia (except with (+) peritoneal signs)

Crohn’s: cobblestone appearance/skip lesions UC: erythema starts in the rectum and extends proximally

Avoid endoscopic procedures in acute disease>perforation/toxic megacolon Biopsy: determine histopathology Treatment 5-ASA products-good for maintainence Sulfasalazine (Azulfidine) Mesalamine (Asacol, Pentasa) Corticosteroids-for acute attacks *primarily used to treat flares Prednisone Methylprednisolone Immunomodulators-for refractory disease 6-mercaptopurine Azathioprine Methotrexate Cyclosporine

Antibiotics-for acute infectious flare-ups Metrodinazole (Flagyl) Ciprofloxacin (Cipro) or levofloxacin (Levaquin) Surgery Crohn’s: reserved for complications; segmental resection UC: can be curative; total proctocolectomy is choice Cancer: UC/Crohn’s patients should undergo colonoscopy screening q1-2 years 8-10 yrs after diagnosis

 INTUSSUSCEPTION General considerations Invagination of a proximal bowel segment into a distal segment Most commonly in children: 95% of cases Risk factors in children: Recent viral enteritis Cystic fibrosis Meckel’s diverticulum Risk factor in adult: neoplasm Clinical features “currant jelly stool” Crampy abdominal pain Nausea, vomiting and/or diarrhea (+)palpable sausage-like mass on abdominal exam Diagnosis Children: barium/air enema Adult: confirmed by CT scan Treatment Children: barium/air enema=diagnostic & therapeutic Adult: abdominal exploration & resection of intussuscepted segment

 IRRITABLE BOWEL SYNDROME General considerations Functional disorder w/o an etiology Most common cause: chronic/recurrent abdominal pain in the US Affects up to 20% of adults W>M Symptoms associated with menses/stress Clinical features Symptoms vary widely Constipation, diarrhea or mixed bowel habits

Lower abd pain typically relieved with defecation Alarm features Anemia, weight loss, FH colon CA, major symptom change or 1st symptom after the age of 50 Diagnosis Diagnosis of exclusion Colonoscopy should be done in anyone with alarm features Treatment Strong provider-patient relationship is key Reassurance Fiber therapy If loose stool>polycarbophil If firm stool>methylcellulose Antispasmodics Function: decrease sigmoid colonic contractions Dicyclomine (Bentyl), hyoscyamine (Levsin) Contraindications for use of anti-spasmodics: Glaucoma GI obstruction Myasthenia gravis Obstructive uropathy Antidepressants Based on data that 25% patients may benefit Nortriptyline (Pamelor), amitriptyline (Elavil) Psychological Cognitive behavioral therapy Hypnosis

 INTESTINAL ISCHEMIA General considerations Predisposing conditions Older age Arterial embolus conditions (arrhythmias, heart failure, valve) Arterial occlusion conditions (trauma, vasculitis, AAA) Low-flow states (sepsis, dialysis) Extensive surgery of esophagus, stomach, duodenum Superior Mesenteric artery=most common site Clinical presentations Acute: pain out of proportion to exam Chronic: abdominal angina 30 minutes postprandially

Hypotension, tachycardia, decreased bowel sounds Diagnosis Leukocytosis Hemoconcentrated Metabolic acidosis Plain film: air-fluid levels, thumb-print sign Multidetector CT angiography-95% sensitivity/specificity Treatment Resuscitation: volume replacement, optimize cardiac output Broad-spectrum anbiotics Ciprofloxacin (Cipro) and metronidazole (Flagyl) Peperacillin & tazobactam (Zosyn)

 ACUTE LOWER GI BLEED General considerations Bleeding source is below the ligament of Treitz (UGIB is above it) Patients are usually older and present with painless hematochezia If orthostasis is present, consider a brisk UGIB Most common colorectal cause: diverticulosis Also: internal hemorrhoids, neoplasms, ischemic colitis Risks: Older age Inflammatory bowel disease Prior bleed Radiation therapy NSAID use Clinical features Weight loss/∆ bowel habits>consider malignancy Bleeding s/p radiation>radiation colitis Hx IBD w/ bleeding>acute flare up colitis Intermittent bleeding, BRBPR, pregnancy>hemorrhoids

Brown stool mixed w/blood>rectosigmoid/anal source Large volume bright red blood>colonic source Melena>proximal to ligament of Treitz Diagnosis Mild bleeding: manage outpatient basis Volume replacement as needed NG tube to exclude upper tract source Flex sig/anoscopy-anorectal/distal colon source

Colonoscopy for other bleeding source If no source on colonoscopy: UGI endoscopy LGI and UGI source negative: capsule endoscopy Nuclear scintigraphy/angiography: reserved for persistent/rapid bleeds Treatment Medical resuscitation Colonoscopic treatment of focal sources Angiographic embolization for rapid bleeds Indications for surgery Malignant lesions Diffusely bleeding lesions Recurrent diverticular hemorrhage

 COLONIC POLYPS General considerations Present in 30% of adults >50yrs old Two classifications: nonadenomatous or adenomatous (neoplastic) Three types: sessile, flat, pedunculated Nonadenomatous Account for 90% of large bowel Found in 50% of adults > 60 yrs old Adenomatous Have malignant potential Malignancy risk increases with size (>2cm-highest risk) Clinical features Generally asymptomatic (+)stool occult blood/hematochezia Diagnosis Preferred method of diagnosis: colonoscopy Flexible sigmoidoscopy detects 50-60% of polyps/cancer Treatment Endoscopic polypectomy=↓ mortality/incidence of colorectal CA Surgical resection indicated when endoscopic resection not possible

 COLORECTAL CANCER General considerations 3rd most common cancer in the US/2nd leading cause of cancer death 95% of adenocarcinomas arise from adenomas Sites of development: 38% cecum, 35% sigmoid, rectal Risk factors Age: 90% of cases occur in patients >50yrs old Family history of neoplasia/colorectal CA/familial polyposis History of inflammatory bowel disease Clinical features Slow-growing/present for years before symptoms develop Asymptomatic tumors-detected by fecal occult blood testing Fatigue/weakness>iron-deficiency anemia ∆ bowel habits circumferentially Hematochezia Tenesmus Urgency Diagnosis/Screening Colonoscopy-diagnostic procedure of choice Barium enema/CT reserved for patients who: Colonoscopy unable to reach cecum Nearly obstructing tumor prevents passage of scope

Screening options beginning at age 50 for average-risk individuals Colonoscopy Q10 yrs Flex sig Q5yrs CT colography Q5yrs Barium enema Q5yrs FOBT Annually

CEA -to monitor patients; not detection (CEA> 5ng/ml=poor prognosis)

Treatment Surgical resection Stage I: no adjuvant therapy 5-year survival: >90% Stage II: node-negative disease 5-year survival rate: 80% Adjuvant chemo is beneficial for high-risk Stage II

Stage III: node-positive disease 5-year survival: 30-50% s/p surgical resection (+)adjuvant chemo recommended: 5-FU & leucovorin Stave IV: mets disease Median survival: 6 months; adjuvant chemo w/ capecitabine Chemoprevention-NSAIDs including aspirin Dietary prevention: more fruits/vegetables/fiber; No reduction 3-8 yrs on follow-up

 OBSTRUCTION  SMALL BOWEL OBSTRUCTION General considerations 60% related to postoperative adhesions 10% related to hernias Other causes: neoplasms, IBD, volvulus Clinical features Early: crampy, colicky abdominal pain which is diffuse; (+)vomiting (+)hyperactive bowel sounds Late: steady abd pain which is better localized (+)quiet abdomen with no bowel sounds Diagnosis Imaging: (+)dilated bowel loops and air fluid levels on abd x-ray CT help determine etiology, gas in wall indicates strangulation Treatment NG tube placement for decompression Narcotic pain medication IV hydration Antiemetics Surgery: for strangulated; avoid in paralytic ileus

 LARGE BOWEL OBSTRUCTION General considerations Slower and less dramatic in presentation Most secondary to neoplasm Other causes: strictures, hernia, volvulus, fecal impaction Clinical features Abdominal distention, anorexia, nausea, vomiting Feculent vomiting-late stage Absence of bowel sounds in late stage Diagnosis

Abd x-ray: free air, bird’s beak volvulus CT scan Treatment: surgery more likely with LBO; endoscopy may reduce volvulus Patients likely to get some type of ostomy: temp vs permanent

 TOXIC MEGACOLON General considerations True emergency Extreme dilatation & immobility of the colon Can be a complication of UC, Crohn’s, pseudomembranous colitis High risk of perforation Clinical features Fever, severe cramps, abdominal distention (+)abdominal rigidity and rebound tenderness (+)patients often in shock with hypovolemia Diagnosis: Abdominal x-ray demonstrates colonic dilatation >6cm Treatment Broad-spectrum antibiotics Ampicillin-sulbactam (Unasyn) Levofloxacin (Levaquin) + metronidazole (Flagyl) Cefazolin (Ancef) + metronidazole (Flagyl) NG suctioning & colonic decompression IV fluids Surgery: possible total colectomy/colostomy

 HERNIAS General considerations Defined as protrusion of any viscous from its proper cavity Reducible: able to return contents of hernia into abdominal cavity Incarcerated: contents of hernia sac cannot be returned into abdominal cavity Strangulated: an incarcerated hernia in which blood supply is compromised

TYPES Umbilical-can be congenital; appears at birth; many resolve on their own; also w/ pregnancy & obesity Hiatal-GEJ/stomach project above diaphragm; causes GERD Incisional: more commonly w/ vertical incisions; F:M=2:1 Inguinal:

Direct: passes through external inguinal ring; rarely passes into scrotum Indirect: more common; may pass into scrotum Femoral: least common; passes through femoral ring; ↑ strangulation rate

Clinical features if strangulated: localized sharp, intense abdominal pain Associated with anorexia, vomiting Diagnosis: elevated wbc count, CT/ultrasound can be done Treatment: surgical

 RECTUM  ANAL FISSURE General considerations Occur at any age; frequently affects young adults M=F Most occur at posterior midline Any fissures off midline=red flag for neoplasm/Crohn’s/syphilis/HIV Clinical features/Diagnosis Diagnosis based on history and inspection Presentation: severe anal pain exacerbated by bowel movements Diagnostic triad on physical exam: The fissure itself “sentinel” skin tag Presence of hypertrophied anal papilla at dentate line Treatment 40% heal with fiber and fluid intake Symptomatic relief: warm sitz baths, especially following BMs Topical nitroglycerin/diltiazem gel to reduce sphincter tone Lateral internal sphincterotomy for those who fail medical treatment

 PERIANAL ABSCESS/FISTULA General considerations Most abscesses caused by infections of anal glands Other causes: skin infection, trauma, anorectal surgery, malignancy Fistula: complication of chronic perianal abscess Clinical features Abscess: perianal pain and swelling (+)local erythema, swelling and fluctuance

Fistula: recurrent abscess in same location; persistent purulent drainage from a non-healing chronic abscess Treatment Abscess: local incision & drainage Antibiotic therapy alone w/o I&D is inadequate Antibiotic therapy usually not indicated after I&D Fistula: treatment is surgical

 PILONIDAL DISEASE General considerations An abscess in the sacrococcygeal cleft Associated with subsequent sinus development M:F=4:1 Clinical features Painful, fluctuant area at the sacrococcygeal cleft Treatment Surgical drainage, may be supplemented with antibiotics Subsequent follicle removal and unroofing of sinus tract

 HEMORRHOIDS General considerations Varices of the hemorrhoidal plexus Causative factors: constipation, pregnancy, prolonged straining

Clinical features/Treatment Most common symptom: painless BRBPR External: are visible perianally Treat with analgesics OTC, sitz baths and fiber intake; more severe cases=excision

Classification of Internal hemorrhoids Grades: Findings: Treatment

Grade I Bleed, but (-)prolapse High fiber diet, increased water intake, rubber band ligation, sclerotherapy

Grade II Prolapse but reduce Dietary modification, spontaneously rubber band ligation, sclerotherapy

Grade III Protrude and require Dietary modification, digital reduction rubber band ligation, sclerotherapy, surgical hemorrhoidectomy

Grade IV Chronically protrude; Urgent/surgical irreversible; risk hemorrhoidectomy strangulation

 ANAL CANCER General considerations Rare, but 80% cases related to HPV virus Majority are squamous cell carcinoma Clinical features: most common symptoms are bleeding, pain and noted local tumor Diagnosis: CT/MRI to identify regional lymphadenopathy/metastasis Treatment <3cm-wide local excision Abdominoperineal resection w/ or w/o chemo

 DIARRHEA General considerations Classifications -Acute vs Chronic: acute=<2weeks; Chronic=presents for >4weeks -infectious vs noninfectious -inflammatory vs noninflammatory: noninflammatory=no blood; inflammatory=bloody diarrhea

Causes of Acute: Inflammatory Noninflammatory CMV rotavirus Entamoeba histolytica norovirus E.coli 0151: HS Giardia lamblia Shigella Cryptosporidium Campylobacter jejuni Staph aureus Salmonella clostridium perfringens Vibrio cholera

Causes of Chronic: Osmotic-water is drawn from the body; symptoms decrease w/fasting Medications: lactulose/antacids/sorbitol Secretory-large volume loss; little change w/ fasting Hormone-mediated: VIPoma, gastrinoma Laxative abuse Inflammatory conditions such as UC & Crohns Motility disorders: scleroderma, IBS, DM, hyperthyroidism Malabsorption: celiac disease, chronic pancreatitis Chronic infections: Giardia lamblia, entamoeba histolytica, cryptosporidium, CMV Clinical features Greasy/malodorous stool-malabsorptin disorder Dysentery (with blood/pus)-inflammatory disorder (+)abdominal pain-IBS or IBD Community outbreaks-viral etiology/common food source Diagnosis (+)heme positive stool & (+)fecal leukocytes-inflammatory bowel disease (+)fecal fat-malabsorption Send stool culture for bacterial agents/parasites/toxins Mucosal biopsy to r/o inflammatory process

Treatment Antidiarrheal agents Reserved for mild-moderate disease Loperamide (Immodium) 4mg daily then 2mg/d s/p BM Opioids helpful to decrease urgency and fecal liquidity indicated in chronic, intractable diarrhea contraindicated in bloody diarrhea high fever systemic toxicity Empiric antibiotics is not indicated in acute diarrhea should be considered in immunocompromised/dehydration

 METABOLIC DISORDERS  PHENYLKETONURIA General considerations Rare, autosomal recessive Unable to metabolize phenylalanine Unable to convert phenylalanine>tyrosine Diagnosis Screening at birth Diagnosis after age 3 leads to brain damage Treatment Manage low phenylalanine diet Tyrosine supplementation Consequences if untreated: developmental delay and movement disorders

 LACTOSE INTOLERANCE General considerations Lactase=enzyme produced in small intestine to digest lactose Clinical features Nausea, bloating, flatulence, diarrhea s/p ingestion of dairy products Management Avoid milk/dairy products Use OTC lactase enzyme tablets/drops

Vitamin Function Deficiency Toxicity A Vision/antioxidant Night blindness Skin disorders Dry skin Hair loss

D Ca+/PO4+ regulation Rickets-children ↑Ca+ Osteomalacia-adults Renal stones

E Cell aging/vascular Hemolytic anemia Inhibits Vit K integrity

K Clotting Bleeding Anemia/jaundice

Niacin Energy/fat Pellagra (3 D’s) Flushing metabolism Diarrhea Dermatitis Dementia

Thiamine Carbohydrate Dry beriberi: Lethargy, ataxia (B1) metabolism -neuropathy -poor coordination Wet beriberi: -cardiac dysfunction Wernicke encephalopathy

Pyroxidine Protein metabolism Dermatitis/cheilosis Photosensitivity/peripheral (B6) neuropathy

Riboflavin Oxidation-reduction Cheilosis/glossitis Not reported (B12)

Vitamin C Antioxidant/collagen Scurvy-fatigue, Renal stones/diarrhea (ascorbic synthesis depression, poor acid) wound healing

Folate DNA synthesis Megaloblastic anemia N/A