Gastroenterology

Gastrointestinal Bleeds Upper GI Bleeds Etiology  Mallory-Weiss tear  Varices  Gastritis  Ulcer peptic

Signs and Symptoms  Hematemesis(bright red or coffee grounds)  Hypotension  Tachycardia  Bleeding that produces 60cc of blood or more will produce black, tarry stool.

Diagnosis  Gastric lavage with normal saline  Rectal exam with fecal occult blood testing  CBC  Endoscopy  Arteriography

Treatment  Depends on the etiology and severity  IV fluids and blood  Endoscopy with epinephrine injection  IV proton pump inhibitor  Most Mallory-Weiss tears resolve spontaneously

Lower GI Bleeds Etiology Cancer or polyps Upper GI bleed ( need to rule it out) Colitis Angiodysplasia Hemorrhoids Angiodysplasia

Signs and Symptoms  Bright red blood per rectum(hematochezia)  Melena (black or maroon tarry stool)  Signs of blood loss  Diarrhea( as seen with colitis)

Diagnosis Gastric lavage to rule out upper GI source Rectal exam CBC Coloscopy Arteriography

Treatment  Fluids  Blood  Embolization or surgery

Diarrhea Abnormal passage of fluid or semisolid with increased frequency. History 1)Quantity of diarrhea  Small bowel involvement usually large volume, watery diarrhea  Large bowel involvement usually small –volume diarrhea

1)Length of symptoms  Acute < 2 weeks  Persistent > 2 weeks  Chronic > 4 weeks 2)Associated Sx : Fever, Chills, abdominal pain, nausea, vomiting and weight loss

Food intake prior to onset of diarrhea Travel history Medications Recent antibiotic use or hospitalization increasing risk for clostridium difficile colitis Lactose intolerance.

ACUTE DIARRHEA Work –up Fecal leukocytes may be suggestive of infectious or inflammatory causes. Stool culture for enteric pathogens Stool test for C.difficile toxins ( for pseudomembranous colitis. Stool exam for oval and parasites

Common Infectious Pathogens Bacterial a)Noninvasive  Staphylococcus aureus  Bacillus cereus  Vibrio cholerae  Enterotoxigenic E coli

b)Invasive : Campylobacter associated with Guillain-Barre syndrome. Salmonella( raw egg),Shigella, enterohemorrhagic E. Coli, C.difficile. c) Viral: Rotavirus, Norwalk. d)Protozoa: Giardia lamblia (after hiking trip) Entamoeba histolytica

Bloody diarrhea : CASES  Campylobacter  Amoeba ( E.Histolytica)  Shigella  E.Coli  Salmonella

Scenario 1 A patient vomits within 6 hours of eating something with mayonnaise ( potato salad at a picnic on a hot day.

Scenario 2 &3  A patient has vomiting /diarrhea after eating reheated rice from letfover chinese food.  A patient has vomiting and severe watery diarrhea after eating spoiled shellfish.

 A patient has flatulence and foul-smelling diarrhea after a camping trip.  A patient has watery diarrhea following a recent course of antibiotics.

Management Oral or intravenous rehydration Electrolyte replacement Antibiotic therapy when infection suspected. Antimotility agent (loperamide) in noninfectious diarrhea.

Chronic Diarrhea  Osmotic : Ingestion of nonabsorbable solute leading to osmotic water in the stool( lactose intolerance.  Secretory :Oversecretion of water by the small and large bowel which may be caused by bacteria,bacterial toxins, laxative.

Inflammatory: Gastrointestinal mucosal irritation and inflammation leading to an exudative diarrhea( IBD). Malabsorption : A problem with either digestion (i.e., lack of digestive enzymes or bile acids) or transport ( problem with the small bowel mucosa).Examples : chronic pancreatitis, bile acid malabsorption

Workup Fecal electrolytes and calculation of osmotic gap. D-xylose test 72 –hour fecal fat analysis

Constipation Definition : Stool frequency < 3 times per week. Etiology Low fiber, low fluid intake Obstruction Disturbed colonic motility Medications Hypothyroidism

Treatment Increase fiber to 30 g/day Increase fluid intake Bulk-forming and emollient laxatives

Gastroesophageal Reflux Disease Definition : Reflux of acidic gastric contents into the esophagus. Causes of Gerd  Relaxed or incompetent lower esophageal sphincter (LES)  Hiatal hernia  Delayed gastric emptying  Decreased esophageal motility

Causes of Lowered LES tone  Foods :coffee, chocolate  ETOH  Cigarettes  Drug : Nitrates, Ca channel blockers  Hormones : Estrogen,progesterone

Causes of delayed gastric emptying:  Diabetes mellitus  Gastroparesis  Gastric outlet obstruction  Fatty foods

Signs and Symptoms  Substernal burning pain  Dysphagia  Hypersalivation ( water brash)  Cough ( particularly noctural

Diagnosis A trial of proton pump inhibitor will be given to relieve symptoms without further work-up. Treatment 1- Lifestyle modification  Elevate head of bed  Discontinue foods that decrease LES tone ;avoid foods <3 hours before bed

2-Pharmacologic  H2 blocker  Proton pump inhibitor 3- Surgical  Surgical correction such as fundoplication

Complications of GERD  Esophagitis :Esophageal damage, bleeding and friability due to prolonged exposure to gastric contents  Peptic stricture : occurs in about 10% of patient with GERD  Barrett’s esophagus  Esophageal Cancer

Peptic Ulcer Disease Duodenal Ulcer Pathophysiology : increase acid production. Etiology  H. pylori  NSAIDs/Steroids :inhibiting mucosal barrier production  Zollinger-Ellison syndrome

Clinical Features  Burning gnawing epigastric pain that occurs with an empty stomach :pain relieved within 30 min by food  Nighttime awakening ( when stomach empties)  Nausea,vomiting  Associate with blood type 0

Diagnosis:  Endoscopy  H.pylory 1-Endoscopy with biopsy 2-Seroloy : Anti-H.Pylori IgG indicates current or prior infection. 3-Urease breath test

Treatment of PUD Discontinue NSAIDs, steroids and smoking Triple therapy for H.pylory(proton pump inhibitor, amoxicillin and clarithomycin) Surgery is indicated when ulcer is refractory to 12 weeks of medical treatment or if hemorrhage,obstruction or perforation is present.

Gastric Ulcer Definition : Ulcer located in the stomach Pathophysiology: decreased protection against acid :normal or low acid production. Etiology H. pylori NSAIDs/steroids

Clinical features  Burning gnawing epigastric pain that occurs with anything in the stomach :pain is worst 30 min after food.  Anorexia /weight loss  Vomiting  Associated with blood type A

Diagnosis Via endoscopy ; 3 % of GUs are associated with gastric cancer. Treatment Same as for DU

Hepatitis Definition Systemic infection or inflammation of the liver due to viral agents,toxins or alcohol. Etiology Viral hepatitis A,B,C,D, E or G ETOH Toxin:Acetaminophen, aflatoxin

Signs and Symptoms Right upper quadrant pain Nausea,vomiting,malaise,fever jaudice

Hepatitis A virus Definition RNA virus Spread by fecal-oral route 15 to 50-day incubation No chronic carrier or infection state

Diagnosis Anti-HAV IgM=acute infection Anti-HAV IgG =immunity from prior infection Treatment Treatment is symptomatic Self-limited,no progression to chronic liver disease

Prevention  Anti-HAV immunoglobulin in 90% effective if given within 2 weeks  HAV vaccine is given to all with chronic liver disease ( especially hepatitis C ) travel to high- risk countries, high-risk behavior, high-risk communities.

Hepatitis B Definition DNA virus Spread by percutaneous or mucous membrane exposure to blood, semen and saliva 45-to -160 day incubation

Diagnosis Hbs Ag positive = infection is present Anti-HBc IgM =the infection is acute( window period) Anti-HBs IgG =past infection or vaccine( indicates immunity)

Prevention Vaccine Hepatitis B immune globulin Treatment Lamivudine Complications 1 % will develop fulminant hepatic necrosis 10 % of adults will develop chronic carrier state or chronic hepatitis with increased risk of Ca

Hepatitis B exposure Scenarios Exposed newborn :give HBIG vaccine Infected Blood exposure :test for hepatitis B and if negative,give HBIG alone

Hepatitis C virus Definition RNA virus Spread by blood and body fluid contact ( common from past blood transfusions and tattoos, IV drugs) Incubation 15 to 160 days Most common hepatitis in the U.S

Diagnosis Anti-HCV IgG presents 1 to 6 months after infectivity and indicates chronic or past infections PCR for hepatitis C RNA measures viral load or disease activity. Treatment Interferon and ribavirin