Gastrointestinal System/Nutrition Inflammatory bowel disease (Crohn’s/UC) ▪ IBD → recurrent abd pain, fever, fatigue, (bloody), weight loss, extra-intestinal sx o Antibodies: P-ANCA (UC), ASCA (Crohn dz) o Complications: toxic megacolon, obstruction, perf, abscess, fistulas, colon CA (>UC) o Tx: 5-ASA (sulfasalazine for colon, mesalamine for small bowel), glucocorticoids, IVF, immune modulators (azathioprine, MTX, cyclosporine, infliximab)

Ulcerative colitis • Chronic mucosal inflammation, almost always starts in rectum, inflammation extends continuously (no skip lesions) for variable extent • Types: o Ulcerative procitits – bowel inflammation limited to rectum (usually <6in); mildest form o Proctosigmoiditis – inflammation involving rectum and sigmoid colon o Left sided colitis – continuous inflammation that begins at rectum and extends to splenic flexure of colon o Pancolitis – inflammation affecting entire colon • Clinical presentation: bloody, mucous diarrhea, fever, abd pain, tenesmus, weight loss • Dx: o Sigmoidoscopy, colonoscopy: mucosal erythema, granularity, friability, exudates, ulcers • Complications: toxic megacolon, colonic perforation, increased risk of colon CA (after 8yrs colonoscopy every 2yrs)

Crohn’s disease • Chronic mucosal inflammation affecting any part of GI tract w/skip lesions classically through affected terminal ileum/colon o Transmural inflammation, bowel wall thickening, linear ulcerations, submucosal thickening  cobblestone pattern • Patterns: inflammatory (80%), structuring (10%), fistulizing (10%) • Clinical presentation: fever, abd pain, non-bloody diarrhea, fatigue, weight loss, anorectal fissures/fistulas/abscesses • Dx: o Sigmoidoscopy/colonoscopy (mucosal erythema w/nodularity or ulcers that are deep/longitudinal, cobblestoning, skip areas, ULCERATIVE CROHN’S strictures, fistulas) COLITIS DISEASE o Serologic markers (ASCA – ab against saccharomyces cerevisiae) No skip lesions Skip lesions o CT enterography (suspicion of small bowel involvement) Affects colon only Affects mouth to • Complications: anus o Intestinal obstruction (often w/stricture formation) Curative via Not definitively o Intestinal fistulas to bowel/bladder/vagina/skin + abscess formation colectomy curative o Increased risk of colon CA

Treatment of Crohn’s & UC • Medications: 5 aminosalicylates (5-ASA), corticosteroids, immunosuppressants, abx (metronidazole (flagyl), cirprofloxacin), TNF inhibitors • Surgery o Colectomy w/resulting ostomy ▪ Curative in UC (limited to colon) ▪ Non-curative in CD (skip-lesions  can have dz anywhere mouth to anus) o Colon resection ▪ Common in CD pts w/stricture, recurrent fistulas and abscesses

Irritable bowel syndrome Acute abdomen ▪ → chronic abd pain, altered bowel habits, abd bloating, w/ no ▪ Peritonitis / ascites → perf, ruptured structural or biochem disorder ulcer/appendix/diverticulitis, pancreatitis, SBP (cirrhosis)

Bowel obstruction Appendicitis ▪ Obstruction → most commonly due to adhesions, ▪ Periumbilical to RLQ pain, N/V, anorexia, fever, pain at malignancy, then hernia → xray, US, CT McBurney point, (+) Rosving, Psoas, Obturator signs ▪ CT w/ contrast, US, can do MRI in pregnancy ▪ Appendectomy ▪ Antibiotics ▪ Gastrointestinal bleeding (Upper GI Bleed) • Etiologies: PUD, erosive esophagitis/gastritis, esophageal varices, Mallory-weiss syndrome, arteriovenous malformation, malignancy • Hx: hematemesis, coffee-ground emesis, melena, hx of /retching, hx of salicylate, glucocorticoid use, NSAID, anticoagulant use, EtOH abuse, hematomchezia 14% • PE: o Visual inspection of vomitus for bloody, maroon, coffee-ground appearance most reliable way to dx o VS: hypotension, tachycardia, paradoxical bradycardia o Carful ear, nose, throat inspection may reveal occult bleed o Abd exam: tenderness, masses, ascites, organomegaly o Rectal exam: presence of blood and appearance (bright red vs. maroon vs. melanotic) o Signs/sx’s of dz  ▪ Shock – diaphoresis ▪ Liver dz – spider angiomas, palmar erythema, jaundice, gynecomastia ▪ Coagulopathy – petechiae, purpura • Labs: CBC, BUN/Cr, CMP, glucose, coagulation studies, lactate, ECG (BUN/Cr ratio >30 suggests UGI) • Imaging: o XR studies limited value, Barium CI (may inhibit EGD) o EGD for direct visualization of source of bleed, dx study of choice o NG intubation and aspiration both dx and therapeutic ▪ Visual inspection of bloody, maroon, coffee-ground aspirate verifies UGI ▪ Negative NG does not exclusively exclude UGI source • Risk stratification: o Low risk: no major comorbidities, no hx of red hematemeisis, no hematochezia, negative NG aspirate, hemodynamically stable at presentation, normal labs o High risk: advanced age, comorbidities, red hematemeisis, hematochezia or melena, positive NG aspirate, hemodynamically unstable, abnormal labs • Initial tx: stabilization • Other tx: o Blood transfusion: transfuse <7g/L (<9g/L in elderly pts) o Correct coagulopathy: correct if INR elevated, platelets <50,000, severe bleed o Omeprazole: 80mg IV bolus than infusion of 8mg/hr IV; labeled use for ulcer bleeding o Octreotide: 50mcg bolus than 25-50mcg/hr IV; unlabeled use for lower range, use lower doses for elderly o Abx: Ciprofloxacin 400mg IV or ceftriaxone 1g IV; use for cirrhotic pts o EGD tx: used for direct visualization and administration of hemostatic therapy (clips, thermocoagulation, sclerosant injections, epi injections); should be done w/in 24hrs o Balloon tamponade: short-term solution for life-threatening variceal bleeding, consider intubation before procedure ▪ Sengstaken-Blakemore tube: 250cc gastric balloon, esophageal balloon, and single gastric suction port ▪ Minnesota tube: has added esophageal suction port above esophageal balloon ▪ Cx: mucosal ulceration, esophageal/gastric rupture, asphyxiation from tracheal compression o Surgery: indicated for pts w/bleeds refractory to pharmacologic and EGD tx • Options; shunts, esophageal transection, gastro-esophageal junction devascularization, percutaneous embolization Lactose intolerance Gastric Cancer • Inability to digest lactose into glucose and galactose ▪ High incidence in Korea, Japan, and China secondary to low levels of lactase enzyme in duodenal brush ▪ Usually occurs after age 60 border Etiologies • Prevalence: very common (25% white Americans, 75-90% ▪ Pickled foods, Salted foods, Smoked foods Asian Americans) ▪ H. pylori • Clinical presentation: loose stool, abd bloating and pain, ▪ Atrophic gastritis, Polyps, Radiation flatulence, nausea, borborygmi Signs & symptoms • Dx: ▪ Early disease is asymptomatic o Hydrogen breath test – DX TEST OF CHOICE ▪ Indigestion, nausea, early satiety, anorexia, and weight loss ▪ Pts administered lactose after overnight ▪ Advanced: pleural effusions, SBO, bleeding fast ▪ Palpable stomach, Hepatomegaly, Pallor ▪ Expired air samples collected before and at ▪ Virchow’s nodes or Sister Mary Joseph nodes 30min intervals for 3hrs Workup ▪ Assess rise in hydrogen gas concentrations ▪ EGD, Endoscopic US, Barium swallow, CT/MRI (rise in H+ concentration = lactase Management deficiency) ▪ Depends on stage  Resection, chemo, radiation, adjuvants if o Trial of dietary elimination needed • Tx: dietary adjustment, lactase replacement (lactaid and Prognosis lactrase) ▪ Difficult to cure, most will die of recurrent disease Acute Diarrhea (Less than 2 weeks duration) ▪ Most common causes are infectious agents, bacterial toxins, or drugs ▪ Other causes to consider: Anal sex: Neisseria gonorrhoeae, syphilis, lymphogranuloma venereum, HSV -Noninfectious: drug reaction, UC, Crohn’s, ischemic colitis, fecal impaction, abuse, radiation colitis, emotional stress ▪ Inflammatory o Invasive or toxin-producing bacteria o Causes: shigellosis, salmonellosis, Campylobacter, Yersinia, C. diff, EHEC, Entamoeba histolytica, Neisseria gonorrhoeae, Listeria o Blood, pus, fever = fecal leukocytes usually present o Diarrhea is typically smaller in quantity, associated LLQ cramps, urgency, tenesmus o Workup with stool cultures, C. diff, ova, parasites ▪ Noninflammatory o Viral or noninvasive bacteria o Infectious causes: virus, preformed toxin, toxin producing bacteria, protozoa (ETEC, Staph, Bacillus cereus, Clostridium, viruses, Giardia) -Watery, nonbloody = no fecal leukocytes -Diarrhea may be voluminous o May have periumbilical cramps, bloating, n/v -Prominence of vomiting suggests food poisoning or viral enteritis o Typically, only eval if persists beyond 7 days or worsens ▪ When to Evaluate Further o Signs of inflammatory diarrhea: fever > 101.3, bloody diarrhea, abdominal pain -Passage of > 6 loose stools in 24 hours o Profuse watery diarrhea and dehydration o Frail older patients, Immunocompromised patients, Hospital-acquired diarrhea ▪ Tests indicated: fecal leukocytes, routine stool culture, C. diff if recent hospitalization or antibiotics, 3x ova and parasites if > 10 d, travel, community water outbreak, HIV, MSM ▪ Management o Rehydration: 1⁄2 tsp salt, 1 tsp baking soda, 8 tsp sugar, 8 oz OJ diluted to 1 L with water o Antidiarrheals for mild to moderate illness o Loperamide (opioid) as long as there is no blood, high fever, or systemic toxicity o Bismuth subsalicylates (Pepto Bismol) good for traveler’s diarrhea as it is antibacterial and anti-inflammatory o Empiric antibiotic treatment only for immunocompromised, significant dehydration, mod-severe fever, tenesmus, bloody stools, or presence of fecal lactoferrin  cipro, Septra, or doxycycline o Send to ED for severe dehydration, severe or worsening bloody diarrhea, severe abdominal pain, signs of sepsis, or worsening diarrhea in patients > 70

Chronic Diarrhea (Greater than 4 weeks’ duration - not attributed to viruses or bacteria other than C. diff) ▪ Differential and signs/symptoms o Osmotic (lactose intolerance or other osmotic agents, factitious Mg overuse or laxative use): stool volume changes with fasting, ↑ stool osmotic gap o Secretory (hormonally mediated, factitious, villous adenoma, salt malabsorption, meds): > 1L stool per day, little change with fasting, normal stool osmotic gap, nonanion gap metabolic acidosis, hyponatremia o Inflammatory (UC, Crohn’s, microscopic colitis, malignancy, radiation): fever, hematochezia, abdominal pain, anemia, hypoalbuminia, ↑ ESR or CRP o Meds: SSRIs, cholinesterase inhibitors, NSAIDs, PPIs, ARBs, metformin, allopurinol -Malabsorption: weight loss, elevated fecal fat, anemia, hypoalbuminia o Motility disorders (IBS): systemic disease or prior abdominal surgery -Chronic infections (parasites, AIDS-related) ▪ Workup o Ask if diarrhea occurs at nighttime or while fasting o Exclude causes of acute diarrhea, lactose intolerance, IBS, previous gastric surgery, parasitic infections, meds, systemic disease o Initial tests: CBC, CMP, Ca, P, albumin, TSH, vitamin A, vitamin D, INR, ESR, CRP, IgA for Celiac o Stool studies: ova, parasites, electrolytes, fat stain, occult blood, leukocytes or lactoferrin -Consider antigen detection for Giardia and Entamoeba o Consider acid stain for Crypto and Cyclospora o Refer for colonoscopy with biopsy o Further testing: 24-hour fecal fat, neuroendocrine tumors ▪ Management o Loperamide (Imodium) o Diphenoxylate with atropine o Codeine and deodorized tincture of opium: only for intractable chronic diarrhea -Clonidine o Octreotide: for neuroendocrine tumors and AIDS diarrhea o Cholestyramine Polyps Hiatal Hernia • Can be sessile or pedunculated and vary considerably in size ▪ Protrusion of upper portion of stomach into chest cavity due • Polyps occur most commonly in the rectum and sigmoid and to diaphragm tear or weakness decrease in frequency toward the cecum. ▪ Type 1: • Multiple polyps may represent familial adenomatous o Sliding hernia  GE junction and stomach slide into polyposis mediastinum • About 25% of patients with cancer of the large bowel also o Most common, increases reflux, treat the same as have satellite adenomatous polyps GERD • Adenomatous (neoplastic) polyps are of greatest concern ▪ Type 2: o Tubular adenomas, tubulovillous adenomas o Rolling hernia  fundus of stomach protrudes (villoglandular polyps), or villous adenomas. through diaphragm with GE junction remaining in its o Likelihood of cancer is related to size, histologic anatomic location type, and degree of dysplasia  a 1.5-cm tubular o Surgical repair to avoid complications adenoma has a 2% risk of containing a cancer vs a 35% risk in 3-cm villous adenomas Obesity o Serrated adenomas = more aggressive ▪ Overweight = BMI 25-29.9 • Nonadenomatous (nonneoplastic) polyps ▪ Obesity = BMI > 30 greater risk of DM, stroke, CAD, death o Hyperplastic polyps, hamartomas (see Peutz-Jeghers ▪ Pharmacologic options  Catecholaminergics (phentermine, Syndrome), juvenile polyps, pseudopolyps diethylpropion, mazindol): short-term use only o Inflammatory polyps and pseudopolyps occur in ▪ Bariatric surgery BMI > 40, or > 35 if obesity complications chronic ulcerative colitis and in Crohn disease of the are present -Results in significant reduction in deaths from colon. obesity o Multiple juvenile polyps (but not sporadic ones) convey an increased cancer risk. The specific number of polyps resulting in increased risk is not known. Esophageal Esophagitis Motility disorders – achalasia ▪ Most common = GERD ▪ Sx: Dysphagia or both solids and liquids (also weight loss, ▪ 2nd most common = infections in immunocompromised - dehydration, regurgitation) candida, CMV, HSV ▪ Dx:  *Esophageal manometry = gold standard*, will show ▪ Risk factors: pregnancy (GERD), smoking, obesity, ETOH, increased LES pressure >40mmHg and decreased chocolate, spicy foods, meds (NSAIDs, beta blockers, CCBs) ▪ Tx:  Decrease LES pressure, botox injection for temporary ▪ Candida esophagitis: relief (6-12 months), nitrates, CCBs, pneumatic dilation of o Linear yellow-white plaques LES, esophagomyomectomy o Treat with PO fluconazole ▪ Most common motility disorder presenting w/dysphagia ▪ CMV esophagitis: o Large superficial shallow ulcers o Treat with ganciclovir Zenker’s Diverticulum ▪ HSV esophagitis: • Progressive out-pouching of pharyngeal mucosa just above o Small deep ulcers upper sphincter o Treat with acyclovir • Distal diverticula assoc. w/motility disorders ▪ Eosinophilic esophagitis: • Sx:  Occur >50yo, transfer dysfunction, halitosis, feeling of o Atopic disease, endoscopy shows multiple neck mass corrugated rings +/- white exudates • Dx:  Barium swallow (collection of dye behind esophagus) o Treat with steroids via inhaler without spacer • Tx: Observation if small and asymptomatic, ▪ Pill induced esophagitis: diverticulectomy, cricopharyngeal myotomy o Most commonly caused by prolonged pill contact with esophagus o Common offenders: NSAIDs, bisphosphonates, iron, Mallory Weiss Tear potassium-chloride, abx (doxycycline, tetracycline, • A tear of the distal esophagus at the gastroesophageal clindamycin), BB’s, CCB’s, vitamin C junction, typically occurring after a bout of vomiting ▪ Caustic (corrosive) esophagitis: • Major cause of upper GIB o Ingestion of corrosive substances: alkali, lue, bleach, • Risk Factors  Underlying portal HTN  acids, HCL diagnose with endoscopy • Sx  Middle aged male presenting with hematemesis, may o Treat with supportive measures, pain meds, IV fluids have recent h/o alcohol ingestion • Dx  Endoscopy is test of choice • Tx  Most will resolve bleeding spontaneously o May require injection or thermal coagulation • Prognosis o Risk of rebleeding

Esophageal Neoplasms Esophageal Varices ▪ Squamous cell (*90-95% worldwide*): associated with ▪ Dilation of gastroesophageal collateral submucosal veins tobacco & ETOH, achalasia, hot beverages, exposure to ▪ Complication of *portal vein HTN* noxious stimuli, men, nitrates (decreased risk: NSAIDs/coffee) ▪ 5-11% UGIB (can lead to hypovolemia if severe) o Peaks age 50-70, more common: African Americans ▪ Risk factors o Assume in >49yo w/new onset dysphagia o Cirrhosis - mortality rate is 30-50% in first bleed o MC found in upper 1/3 ▪ 90% pts w/cirrhosis develop varices, 30% of ▪ Adenocarcinoma (*50-80% in the US): presents in younger varices bleed, 70% of bleeding varices re- patients and presents early, usually a complication of: bleed in 1st year o GERD/Barret’s, obesity ▪ Mortality rate 1st bleed – 30-50%; mortality o MC found in lower 1/3 rate re-bleed – 33% ▪ Sx Solid food dysphagia, weight loss/chest pain, anorexia, o Portal vein thrombosis in kids cough, hematemesis, Virchow's node (left supra-clavicular) ▪ Sx’s: UGIB (5-11% present as UGIB, hematemeisis, melena, ▪ Dx  Upper endoscopy with biopsy hematochezia), sx’s of hypovolemia (d/t blood loss) ▪ Tx: ▪ Dx: o Esophageal resection, radiation, chemo (5-FU) o Upper endoscopy (enlarged veins) o Commonly spreads to the mediastinum o Red wale markings & cherry red spots ▪ Prevention: *Screen patients with Barret's every 3-5 years* ▪ Tx: o Stabilize patient (large bore IV/transfusion, vitK, FFP) Esophageal Webs o Endoscopic ligation – tx of choice, +/- sclerotherapy • Thin membranes of mucosa and submucosa located in mid to o Pharmacologic: octreotide (vasoconstriction), proximal esophagus vasopressin • Can occur w/Plummer-Vinson syndrome o Balloon tamponade  indicated for bleeding • Dx: Barium swallow refractory to EGD ligation or pharmacologic tx, fast • Tx: dilatation bleeding, temporary management before surgical decompression Schatzki ring ▪ Increased risk of esophageal perforation, • Stricture near GE junction ulceration, aspiration pneumonia • Most common cause of intermittent dysphagia with solid food o Surgical decompression - trans jugular intrahepatic • Commonly associated with hiatal hernia portosystemic shunt (*TIPS*) if endoscopic ligation • Sx: Most asymptomatic, presents with food impaction and pharm does not work, • Dx: Barium swallow ▪ Contraindicated with infection or hepatic • Tx: Dilatation encephalopathy o Devascularization and embolization – indicated for Plummer-Vinson Syndrome severe bleeds or cases of thrombosis • TRIAD: Dysphagia + esophageal webs + iron deficiency ▪ Prevention of re-bleed o • Sx  Atrophic glossitis, angular cheilitis, koilonchias, 70% re-bleed within 1st year o splenomegaly Beta-blockers - treatment of choice in primary • Most common: in Caucasian women 40-70yo prophylaxis of re-bleeds (Propranolol, nadolol) o Isosorbide - long acting vasodilator • Iron repletion may lead to resolution of the dysphagia, o Abx prophylaxis: floroquinolones (norfloxicin), dilation may also be required if significant obstruction, ceftriaxone • Recognition is important due to risk of developing esophageal or pharyngeal squamous cell carcinoma Esophageal Strictures Esophageal Perforation ▪ Thin membranes (mid/upper esophagus) • Most commonly: left posteroalteral wall of distal esophagus ▪ Congenital or acquired (eosinophilic esophagitis) • Causes of perforation: ▪ Leads to dysphagia o Iatrogenic ▪ Develops d/t scarring from GERD, inflammation o Boerhaave’s syndrome: full thickness rupture ▪ Occur in distal esophagus proximal to GE junction o Mc cause sudden, forceful emesis d/t bulimia, EtOH ▪ Sx: Build over years, typically noted w/solids only o Trauma: penetrating more common than blunt ▪ Dx:  Barium esophagram/swallow, r/o malignancy w/EGD o FB, Infection, Tumor ▪ Tx:  Endoscopic dilation of the area o Aortic pathology: aneurysm, aberrant right subclavian artery o GI pathology: Barrett’s esophagus, Zollinger-Ellison syndrome • Sx’s: acute may radiate to back and shoulders • PE: Abd rigidity w/hypotension, fever, tachycardia, tachypnea o Cervical subQ emphysema, Pleural effusions o Hamman’s crunch (air being moved by heart beat) • Dx: XR can suggest dx, CT chest or emergent EGD confirms • Tx: prompt detection, parenteral abx, emergent surgery Stomach GERD Peptic Ulcer Dz • Reflux of gastric contents into esophagus via LES → ▪ PUD mc cause of UGIB heartburn, dysphagia, cough, laryngitis, asthma, chest pain ▪ Gastric ulcer  decreased protective factors (, • Etiologies: bicarbonate, prostaglandin, blood flow) o Decreased pressure of LES: high-fat food, nicotine, o GU more common in elderly, 4% caused by gastric ethanol, caffeine, meds (nitrates, CCB, estrogen cancer or become malignant anticholinergics, progesterone) pregnancy o GU: food-provoked dyspepsia/indigestion; pain 1-2h o Decreased esophageal motility: achalasia, post-meals, weight loss scerloderma, presbyesophagus, DM ▪ Duodenal ulcer  increased damaging factors (acid, ) o Prolonged gastric emptying: medicines o DU 4x more common than gastric ulcers, >90% in (anticholinergics), outlet obstruction, diabetic first portion, typically benign gastroparesis, high-fat food o DU: ulcer-like; acid provoked dyspepsia; relief o Hiatal hernia w/food, antacids, anti-secretory agents; worse • Sx before meals or 2-5h post-meals, nocturnal sx’s o Pain, heartburn, odynophagia, dysphagia, ▪ Etiologies: regurgitation, hyper-salivation, pain and discomfort o H pylori infection with meals, diaphoresis, pallor, n/v o NSAIDs: ASA, indomethacin, ketorolac o Symptoms can be exacerbated by head-down o Zollinger Ellision Syndrome position or increase in intra-abd pressure; may be o Other: EtOH, smoking, stress (burns, trauma, temporarily relieved by antacids surgery), elderly, malignancy, steroids o Radiation may mimic cardiac pain and may occur ▪ Sx with exertion or rest; pain may radiate to one or o Asymptomatic, dyspepsia 80% (burning, gnawing both arms, neck, shoulders, back epigastric pain), sx’s usually worse at night, +/- n/d • Less common presentations: asthma exacerbation, sore ▪ Dx  EGD gold standard throat, ear/nose/throat symptoms, dental erosion, vocal cord o Biopsy r/o malignancy  used in pts with alarm sx ulcers and granulomas, laryngitis w/hoarseness, chronic (>50yo, anorexia, weight loss, anemia, dysphagia) sinusitis, chronic cough o Barium swallow option for pts unable to do EGD • Dx: o EGD, manometry (decreased LES pressure), 24h ▪ H pylori testing: ambulatory pH monitoring (gold standard) o EGD w/bx + rapid urease test = gold standard • Complications: o Urea breath test – H pylori converts urea to CO2, can o Strictures, dysphagia, inflammatory esophagitis, be used to confirm eradiation after therapy Barrett’s esophagus → adenocarcinoma o H pylori stool antigen – >90% specific • Tx: o Serologic antibodies – only useful in dx, not o Rx = avoid triggers, antacids (Tums), PPIs confirming eradication (omeprazole), H2 blockers (Ranitidine/Zantac) ▪ Complications: o Lifestyle modifications – elevation of head of bed, o Bleeding: melena, hematemeisis, dizziness, avoid lying down 3hrs after eating, eat small meals, hematochezia, pallor, weakness, dyspnea, anemia avoid trigger foods, decrease fat and EtoH intake, o Perforation: sudden onset severe diffuse abdominal weight loss, smoking cessation pain, rigid abdomen, rebound tenderness (DU) o Antacids and OTC H2RA’s PRN o Penetration: pain radiation to back, not relieved by o H2RA’s, PPI’s, prokinetic agents food/antacids (GU) o Nissen fundoplication if refractory o Obstruction: vomiting hallmark, cramping abdomen pain, nausea ▪ Tx: o H pylori (+): Clarithromycin + amoxicillin + PPI (CAP) o H pylori (-): PPI, H2RA, misoprostol, antacids, bismuth, sucralfate o vagotomy if refractory, bilroth II associated w/dumping syndrome

Gastric Neoplasms Gastritis • Adenocarcinoma MC worldwide (90%), 4% lymphomas and ▪ Etiologies leiomyosarcomas o H. pylori = most common • Risk factors o NSAIDs = 2nd most common - disrupts mucosal o H. pylori = biggest, salt, cured/smoked/pickled barrier via prostaglandin inhibition foods containing nitrites (converted by H. pylori), o Acute stress (critically ill patients) pernicious anemia, chronic atrophic gastritis, o ETOH, bile salt reflux, meds, radiation, trauma, achlorhydria, smoking, EtOH, blood type A corrosives, ischemia, pernicious anemia, portal HTN o Most common in males >40, presents late ▪ Sx • Sx: o Usually asymptomatic, can cause UGIB o Indigestion, weight loss, early satiety, abdominal (hematemesis & melena) pain/fullness, nausea, post-prandial vomiting, o Epigastric pain dysphagia, melena, hematemesis o Nausea, vomiting, anorexia o Pts often have iron deficiency anemia ▪ Dx o Signs of metastasis: o Endoscopy - shows thick edematous erosions ▪ Virchow's node - supraclavicular <0.5cm, h. pylori testing ▪ Sister Mary Joseph's node - umbilical ▪ Tx ▪ Ovarian mets = krukenberg tumor o H. pylori  *clarithromycin + amoxicillin + PPI*, ▪ Palpable node on DRE = blumer's shelf metronidazole if allergen to PCN ▪ Left axillary lymph node = irish sign o NOT h. pylori --> PPI, antacids • Dx ▪ Prophylaxis: PPI, H2 blockers o Upper endoscopy w/ biopsy o Linitis plastica = diffuse thickening of stomach wall Gastroenteritis due to infiltration (worst kind) ▪ Inflammation of the lining of the intestines caused by a virus, • Tx: bacteria or parasites. o Gastrectomy, XRT & chemotherapy ▪ Viral gastroenteritis is the second most common illness in the (adenocarcinoma and lymphoma) U.S., often a norovirus infection  It spreads through • Prognosis  poor contaminated food or water, and contact with an infected person. The best prevention is frequent hand washing. ▪ Sx: o Diarrhea, abdominal pain, vomiting, headache, fever and chills. Most people recover with no treatment. o The most common problem = dehydration o Dehydration is most common in babies, young children, the elderly and people with weak immune systems. Liver Acute Hepatic Failure • Characteristics: acute liver injury, hepatic encephalopathy, impaired synthetic function (elevated INR, prolongation of PT) • Prognosis determined by presence of hepatic encephalopathy and jaundice o Hyperacute: <7days (good prognosis 36%) o Acute: 7-21 days (good prognosis 7%) o Subacute: 21 days – 26wks (good prognosis 14%) • Etiology: o Clinical Etiology – infectious, vascular, toxic, metabolic o Morphologic classification – massive hepatic necrosis, chronic liver dz, hepatic dysfunction w/out necrosis o Most commonly acetaminophen toxicity (39-46%), indeterminate (14%), drug rxn (12%), Hep B (7%), Hep A (3%)

• Symptoms of Acute Hepatic Failure: o 80-90% destruction before sx o Initially symptoms are nonspecific  fatigue/malaise, lethargy, anorexia, N/V, RUQ pain, pruritus, jaundice, abdominal distention due to ascites • Complications: o Cerebral edema, coagulopathy, hemodynamic instability, respiratory or renal failure, metabolic disturbances, sepsis • Dx: o Labs: ▪ Markedly elevated AST and ALT (>5000 units/L) • Micro-vesicular steatosis (fatty liver of pregnancy) >300 units/L • Will trend downward if condition improving ▪ Elevated bilirubin ▪ Low platelet counts ▪ INR/PT will improve/worsen depending on disease progression ▪ AKI can occur 30-50% o Labs based on disease process  ▪ Acetaminophen: very high AST and ALT, modest increase in bilirubin, high INR ▪ Ischemic hepatic injury: very high AST and ALT, elevated LDH ▪ Hep B: high AST and ALT, ALT>AST ▪ Wilson’s disease: coombs negative, hemolytic anemia, high AST and ALT, low alk phos and bilirubin, rapidly progressive RF, low uric acid levels ▪ Acute fatty liver of pregnancy/HELLP: high AST and ALT, elevated bilirubin, low platelets, hemolytic ▪ HSV : very elevated AST and ALT, leukopenia, low bilirubin o Imaging ▪ CT abd: heterogeneity of liver parenchyma, hepatomegaly, ascites, malignant infiltration, vein occlusion ▪ Doppler US: Budd Chiari, portal HTN, hepatic steatosis, hepatic congestion, underlying cirrhosis ▪ Head CT/MRI: cerebral edema ▪ CXR: pulmonary edema ▪ Echo: cardiac dysfunction o Biopsy (indicated if serology unclear)  performed transjugular, can identify malignancy, autoimmune hepatitis, Wilson, acute fatty liver of pregnancy • Treatment o Tx generally supportive ▪ Admit to ICU, correct metabolic/electrolyte abnormalities, nutritional support o Tx underlying cause o Transplantation • Prognosis o Survival >60% o 40% will survive without need of transplant o Highest cause of death sepsis and cerebral edema o Mortality rate for fulminant hepatic failure w/severe encephalopathy approx. 80%

Viral Hepatitis – Rapid Review • HAV: fecal-oral, shellfish, alone (no carrier), asymptomatic, acute • HBV: o HBsAg: active and chronic infection o Anti-HBs: recovered or immunized o Anti-HBc IgM: early marker of infection, positive in window period o Anti-HBc IgG: best marker for prior HBV o HBeAg: high infectivity o Anti-HBeAb: low infectivity • HCV: IVDA, chronic, cirrhosis, carcinoma, carrier • HDV: dependent on HBV coinfection • HEV: fecal-oral (enteric) high mortality rate among pregnant (expectant) patients, epidemics, o HAV and HEV are fecal-oral: “The vowels hit your bowels” • Autoimmune hepatitis: young females • Alcoholic hepatitis: moderate transaminase elevation, AST>ALT

Hepatitis A Hepatitis B • Transmission: fecal-oral from ingestion; person-person • Transmission: body fluids (blood, , semen, vaginal • Incidence: declined 90% between 1995-2006 most likely due secretions)  Perinatal, sexual, IVDU, blood transfusions to vaccination (2 vaccines children 12-23mo 6mo apart) • Incidence: worldwide problem  1/3 global population • RF’s: institutionalization, daycare, MSM, foreign travel infected, #1 cause of cirrhosis and HCC worldwide o Booster 2-4wks before traveling to endemic areas • RF’s: multiple sex partners, IVDU (India, Africa, Central/South America)) • Incubation period: 1-6mo • Incubation period: 2-6wks • Clinical presentation: • Clinical presentation: o Subacute phase – anorexia, N/V, low-grade fever, o Prodrome – mild flu-like illness myalgia, fatigue, RUQ pain o Icteric phase – dark urine, pale stool, jaundice, pain o Icteric phase – dark urine, pale stools, jaundice • Dx: NAT (detection of anti-HAV IgM ab’s) o Chronic phase – flu-like sx’s (same as Subacute) • Tx: supportive care, post-exposure prophylaxis (if >40yo, o Extra-hepatic manifestations – uticaria, joint pain, pooled gamma-globulin given w/in 2wks of exposure, also polyarteritis, nodosa, glomerulonephritis given to household contacts) • Course of infx: subclinical  icteric  acute  asx chronic • Prognosis: excellent long-term immunity; rarely lasting sx HBV infx  cirrhosis  HCC

• Dx: serologic markers Hepatitis C o HBV DNA = first marker for positive infectivity • Transmission: percutaneous blood exposure, STD (<5%) o HbsAg & HbeAg –chronic infx = HbsAg >6mo • RF’s: transfusion prior to 1992; IVDU, hemodialysis, ▪ HbsAg pos. w/exposure vaccine as well healthcare worker, screen if born between 1945-1965 o Anti-HBc IgM – follows elevation of HBV DNA, • Clinical presentation: often asymptomatic o Recovery – seroconversion to antibodies • Dx: • Tx: o Serologic markers  o Goals –prevention of progression to cirrhosis, ▪ HCV RNA (viral load) – usually seen in liver failure, HCC serum 7-21 days after exposure o Begin tx if HBV DNA >20,000 IU/mL and ALT 2X ▪ Anti-HCV ab (anti-HCVab) – at 1-3months upper limit of normal o Genotypes o PEG-IFN 180mcg subQ injection weekly X48wk ▪ Genotype 1a/b – most common (70%); best  SE’s: depression, suicidal thoughts, poor response to medications and prognosis compliance ▪ Genotype 2 and 3 more difficult to treat o Entacavir 0.5mg PO daily X 48wks • Tx: • Vaccine recommendations  3-part vaccination series at o Alpha IFN + ribavirin for 24-48wks 0, 1, 6mo, all healthcare workers revaccinated if titers o New therapy  achieve SVR (undetectable viral neg load at 12wks) 95-97% • Post-exposure prophylaxis: HEP B immunoglobulin o Harvoni (Ledipasvir/sofosbuvir) – approved for (HBIG) if no previous HEP B vaccination or inadequate Genotype 1a/b Combination pill = X12wks response o Zepatier (Grazoprevir/Elbasvir) – approved for Prognosis: 95-99% healthy, immunocompetent adult pts have Genotype 1a/b and 4 favorable course and recovery completely if compliant w/meds o Solvaldi + ribavirin – approved for Genotypes 2/3 Hepatitis D – must have concurrent infection with Hep B Hepatitis E • Transmission: percutaneous blood exposure, STD • Transmission: fecally – contaminated water within endemic • RF’s: IVDU, multiple sexual partners areas (China, Nepal, Southwest Frances, North African) • Course of infx: Strong association w/HEP B  almost always o Can also be transmitted by animals co-infected (93-95%) • Incubation period: 15-60 days • Dx: serologic markers • Clinical presentation: o Pos. HDV RNA, HDV ag, anti-HDV IgM o Prodrome – mild flu-like symptoms • 3 Genotypes o Icteric phase – dark urine, pale stools, jaundice • Tx: supportive care (fluids), PEG-IFN and Entacavir if co- • Dx: serologic markers infected w/HEP B o Positive HEV RNA, HEV ag, anti-HEV ab (IgM) • Vaccination: no specific vaccine available, HEP B effective • Tx: o Mainly preventative – clean drinking water, good Hepatic carcinoma sanitation, proper personal hygiene ▪ Chronic asymptomatic carriers of HepB are at increased risk o Supportive care ▪ Most cases of HCC are because of either a viral hepatitis o Self-limited, will resolve within 5-6wks infection (hepatitis B or C), metabolic toxins such as alcohol or • Vaccination: given 2-4wks before traveling to endemic areas aflatoxin, conditions like hemochromatosis and alpha 1- • Prognosis: excellent; no risk cirrhosis/fulminant hepatic antitrypsin deficiency failure; long-term immunity following infection ▪ Occurs most commonly in countries where hepatitis B infections are common Alcoholic hepatitis Autoimmune hepatitis ▪ Progressive, inflammatory liver injury assoc. w/long-term • Chronic liver dz of unknown cause; characterized by continued heavy ETOH intake hepatocellular inflammation and necrosis o >6drinks/day for men; >4 drinks/day for women o 20% tendency to progress to cirrhosis o Most common precursor of cirrhosis • Incidence: most commonly occurs in women (15-25yo and ▪ Clinical presentation: 45yo); strong assoc. w/other autoimmune conditions (RA, UC) o Often asx • Clinical presentation: dark urine, pale stools, anorexia o Severe cases have acute onset of jaundice, • PE: hepatomegaly/splenomegaly, scleral icterus, spider hepatomegaly, portal HTN angiomas, ascites, encephalopathy o Impairment of liver function  elevated AST • Diagnosis: (marker malnutrition), low serum albumin, o ALT/AST >5X normal thrombocytopenia, elevated INR (coagulopathy) o +ANA or +ANCA, +anti-SMA (smooth muscle Ab) ▪ PE: hepatomegaly/splenomegaly, peripheral edema and • Treatment: ascites (fluid wave), asterixis (hand flapping), spider angiomas o Corticosteroids (chronic prednisone therapy 20- ▪ Dx: clinical dx, no imaging necessary 40mg/day) ▪ Tx: o Immunosuppressant therapy (often added for flares; o Abstinence of alcohol azathioprine (6MP) 50-100mg/day) o Supplemental vitamins and minerals Wilson Disease ▪ Folate, thiamine, MVT (banana bag in ER) • Autosomal recessive disorder of copper metabolism that ▪ Oral supplementation can be given in office causes excessive deposition of copper in liver, brain ▪ Prevents Wernicke’s encephalopathy • Incidence: usually occurs between 12-23yo • Neurological disorder caused by • Clinical presentation: thiamine deficiency (alcoholics) o Fatigue, ascites, jaundice (neurologic: drooling, gait- ▪ Characterized by confusion, abnormal eye disturbance, tremor, mask-like faces) movements, wobbly gait o Ophthalmologic – Kayser-Fleischer rings (pathopneumonic of Wilson’s – copper deposition in cornea)

Drug-induced hepatitis Non-alcoholic fatty liver disease • Incidence: >900 drugs, toxins, herbs implicated; drugs • Condition caused by fatty infiltration of liver (steatosis) not account for 20-40% fulminant hepatic failure related to alcohol - can result in liver failure • Most common hepatotoxic meds: • Incidence: increasing prevalence due to rise in obesity 90% o Acetaminophen (Tylenol) BMI 38-39 or greater; affects 10-20% Americans; leading o Abx – amoxicillin, cipro, erythromycin, TMP/SMX cause of elevated LFTs in adults o Anti-arrhythmics – amiodarone • RF’s: metabolic syndrome  obesity, glucose o Antifungals – fluconazole, terbinafine (always cause intolerance/DM, HTN, HLD LFT elevation; start topicals for toenail fungal infx • Clinical presentation: typically asx, usually incidental finding fist) • Dx: dx of exclusion  Other causes of hepatitis o Anticonvulsants – carbamazepine, phenytoin, • Tx  Lifestyle modifications – weight loss valproic acid o Avoidance hepatotoxins – alcohol, Tylenol o TB meds – INH, rifampin o Tx HLD – statins, fibrates o OCP’s o Tx DM – A1c goal <7% (glucose >126 but normal A1c o Statins (check LFTs at 3mo and 6mo  if not- put on metformin 500mg 1X daily for prevention) elevated don’t need to recheck, if elevated will o Hepato-protective – betaine, vitamin E, continue to rise; change to Cristor – has least chance ursodeoxycholic acid of elevation) o Herbal meds/weight loss pills – Japanese, Asian Non-alcoholic steatohepatitis populations • Condition characterized by steatosis + inflammation and o Recreational drugs – ecstasy, cocaine hepatocellular ballooning/other evidence of hepatocyte injury • Dx: • Incidence: affects 2-5% of Americans o Medication reconciliation • RF’s: metabolic syndrome  obesity, glucose o Onset usually 5-90 days of starting drugs intolerance/DM, HTN, HLD; NAFLD dx o Asx ALT elevation (if ALT >3X ULN should repeat test • Clinical presentation: w/in 72hrs) o Typically asx, often incidental finding

o May present w/fatigue, mild RUQ pain • Dx: only definitive dx = liver bx (invasive, complications) o Steotest = newer test; calculates fat necrosis score • Tx: same as NAFLD • Prognosis: 15% will progress to cirrhosis

Cirrhosis ▪ Late stage of hepatic fibrosis with changes in hepatic architecture (generally considered irreversible) ▪ Usually hard/shrunken liver, collagen spreads throughout liver ▪ ETOH may stimulate cells to produce more collagen ▪ 2 most common causes in the US are ETOH and HepC, also can be caused by hemochromatosis and NASH ▪ Symptoms: o Anorexia, weight loss, weakness, jaundice, pruritis, UGIB, ascies , spider angiomata, splenomegaly, digital clubbing, asterixis, systemic hypotension ▪ Clinical findings: o Fector hepaticus – musty, “sweat and sour” smell or urine and breath o Impaired estrogen metabolism – palmar erythema, spinder angiomata, hypoganadism/gynocomastia

▪ Diagnosis: o Presence of ascites, thrombocytopenia, spider angiomata predictive of cirrhosis o Predictive scales  Bonacini, Lok o Can be made clinically o Definitive dx made w/bx (gold standard) o Determine underlying cause (will affect tx) o AST/ALT moderately elevated o Alk Phos – elevated o GGT – elevated o Can be made clinically given constellation of symptoms, also can use CT o When diagnosing cirrhosis one needs to determine the underlying cause because it may change treatment o Hepatology should be involved early o Imaging  ▪ Abd imaging may show shrunken, irregular, nodular liver; evidence portal HTN • US most common, usually not sp/sn enough alone ▪ Management o ABSTAIN FROM EOTH o Treat underlying cause ▪ Anti-virals for Hepatitis C ▪ Abstain from ETOH o Vaccinations for Hepatitis A and B if needed o Avoid hepato-toxins ▪ Adjust medications, Avoid APAP ▪ Complications: variceal hemorrhage, portal HTN, acites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatocellular carcinoma, hepatorenal syndrome, hepatopulmonary syndrome, hepatohydrothroax, portal vein thrombosis, cirrhotic cardiomyopathy ▪ Transplant o Definitive treatment for decompensated cirrhosis is liver transplantation (refer early) o Criteria for transplant ▪ Irreversible fatal disease ▪ No absolute contraindications • No active drinking, extrahepatic CA, advanced chronic disease, active sepsis, or unfavorable anatomy ▪ Compliance with long-term care ▪ Financial security o Many specialties involved in listing for transsplant o Allocation by UNOS (United Network of Organ Sharing) ▪ Prognosis o Median survival for compensated pts >12yrs o Median survival for decompensated pts <6mo o Complications + ongoing drinking <50% survival rate at 5yrs

Gallbladder/biliary Cholelithiasis/Colecystitis/Cholangitis ▪ Cholelithiasis → biliary colic w/ radiation to back or R shoulder (80% are cholesterol stones) o Meperidine (Demerol) or NSAIDs, elective cholecystectomy ▪ Cholecystitis → RUQ pain, fever, N/V, fatty food intolerance, jaundice, radiation to back or shoulder, (+) Murphy sign, ↑ leukocytosis w/ L shift o US* (stones, gallbladder wall thickening, dilated ducts), HIDA scan, CT o Refer to hospital → NPO, IVF, opioids or ketorolac, empiric abx, cholecystectomy ▪ Cholangitis → Charcot Triad = fever, jaundice, RUQ pain o + hypoTN and AMS = Reynold Pental → suppurative cholangitis Overview • Two types: cholesterol vs. pigmented o Cholesterol (75%) o Pigmented (25%): black/brown; calcium bilirubinate, other Ca salts • 5 F’s: fat, female, forty, fertile, flatulence

• Clinical presentation: o Obstruction at any level by stones/sludge can causes sxs ▪ Possible locations: common hepatic duct, cystic duct, common bile duct, ampulla of vater o 50% asymptomatic o Other 50%: 35% develop biliary colic, 15% develop acute dz o Biliary colic: contraction of gallbladder during transient obstruction of cystic duct by gallstones ▪ Non-specific sxs: dyspepsia, fatty food intolerance, bloating/flatulence, heartburn, belching o Acute cholecystitis: persistent obstruction of cystic duct leading to inflammation or infection ▪ Sxs: acute onset RUQ pain for several hrs, gradual increase in severity, typically localizes to RUQ/epigastrum, radiation to right lumbar, scapula, shoulder possible, N/V, anorexia, no spontaneous resolution ▪ PE: (+) Murphy sign, fever (mild jaundice, palpable gallbladder less common) ▪ Complications: emphysematous cholecystitis (DM, elderly, immunocompromised), empyema, gangrene, gallbladder perforation o Cholangitis: infection of biliary tract o Pancreatitis: may result from obstruction of distal common bile duct • Diagnosis: o Asx  LFTs: “cholestatic pattern”: increased Alk Phos, increased direct bili, normal/mildly elevated AST & ALT o Biliary colic ▪ Imaging  US (95% sn/sp, 20% if CBD) – stones have bright surface echo and acoustic shadow, EUS and MRCP (accuracy of 90-95% for cholelithiasis and CBD stones) o Acute colecystitis ▪ US – presence of gallstones, pericholecystic fluid, gallbladder wall thickening, (+) US Murphy sign, CBD size (>7mm dilated in adults) ▪ HIDA scan – radionucleotide scan; if gallbladder fills w/isotope AC highly unlikely (not blocked) • Management: o Asx  Monitor ▪ Prophylactic cholecystectomy if increased risk of complications • DM  increased risk of m/m from acute cholecystitis • Calcified (porcelain) gallbladder or large polyps  increased risk for gallbladder carcinoma • Sickle cell: hepatitis crisis • Children • Native Americans  increased risk of gallbladder cancer o Biliary Colic ▪ Surgical  cholecystectomy (open if adhesions, obesity, cirrhosis) o Most pts need to undergo, performed in 24-48hrs following presentation most commonly ▪ Non-surgical • Ursodeoxycholic acid - dissolves gallstone, reserved for non-surgical candidates, life-long administration • Abx  Indicated if fever or leukocytosis o Cover Gram (-) rods and anaerobes, add pseudomonas coverage if previous infx  Zosyn + Flagyl

Large and small intestine Diverticulosis Colorectal CA large outpouchings of muocsa in the colon ▪ Incidence: ▪ Signs & symptoms o 1st most common GI malignancy o Many cases of colonic diverticula are asymptomatic o 3rd most common cancer in US and discovered incidentally -Chronic constipation, o 2nd leading cause of neoplastic death abdominal pain, fluctuating bowel habits o Highest incidence in North America, Europe, o May have mild LLQ tenderness Australia, New Zealand ▪ Management o Incidence increasing in US, but increasing worldwide o May reduce complications of diverticulosis with fiber o Overall lifetime risk 1/20 supplements o Avg. age of dx = 73yo o Most common in men, more common in AA vs. Diverticulitis white ▪ Inflammation of the diverticula caused by obstructing o Nearly 98% adenocarcinoma ▪ Signs & symptoms o Most frequently affects sigmoid colon o Cases range from mild to severe ▪ Pre-disposing conditions: age, gender, race, DM, FHx CRC, o Acute abdominal pain and fever inherited CRC syndromes, IBD o LLQ tenderness and mass o IBD (incidence 60% higher) o Perforation  generalized peritonitis o Adenocarcinoma 10-20X more common in US o Constipation or diarrhea, n/v o Crohn’s w/extensive dz (>1/3 colon) 6-8X increased ▪ Differential: risk o Perforated colonic carcinoma, Crohn’s, appendicitis, o Screening every 1-2yrs, 8-10yrs after IBD onset ischemic colitis, C. diff, ectopic pregnancy, ovarian ▪ RF’s: obesity, low physical activity, tobacco, excessive alcohol, cyst, ovarian torsion high-fat diet, lack of dietary fiber ▪ Workup Polyposis syndromes o CBC may show mild leukocytosis ▪ FAP: familial adenomatous polyposis o FOBT may be positive o Autosomal dominant (chrm 5) ▪ Management o Development of 100-1000’s adenomatous o Mild disease  empiric therapy first (Augmentin, or polyps/CRC by age of 40 metronidazole + cipro, or Septra, want to cover o Polyps distrusted fairly evenly throughout colon anaerobes) (slight increase in distal colon) o Clear liquid diet followed by referral for imaging (CT o Tx: total proctocolectomy with ileostomy colonography or barium enema, don’t want to do ▪ HNPCC: hereditary non-polyposis colon CA (lynch syndrome) this right away due to risk of causing perforation) o Autosomal dominant  MLH1, MSH2, MSH6, PMS2 o Advance diet after 3 days or as tolerated o Multiple polyps (not as extensive as FAP) ▪ Send patients with increasing pain, fever, or inability to o Most common hereidatry CRC (% of cases) tolerate fluids to ED, might need bowel resection o Higher risk for other malignancies – endometrial, ▪ Severe disease  send to ED for abdominal CT ovarian, gastric, SB, hepatobiliary, ureter, pancreatic o Screening - colonoscopy ever 2yrs from 21yo, annually after 40yo Toxic Megacolon ▪ Women – pelvic exams every 1-3yrs from • Extreme dilation and immobility of colon 1yo, annual pelvic exams, transvaginal US, • True emergency endometrial bx after 25yo, consider • Etiologies: prophylactic TAH and BSO o Newborns: Hirschsprung dz o Tx – subtotal colectomy o Adults: UC, C. diff, Crohn’s, pseudomembranous ▪ Clinical presentation: BI bleeding, change in BM habits, colitis, shigella infx , campylobacter infx weight loss, intestinal obstruction, abd pain, iron deficiency • Sx’s: fever, prostration, severe cramps, abd distention ▪ Dx/Screening: SCREENING KEY (early dx = best prognosis) • PE: rigid abd, localized/diffuse/rebound abd tenderness o Colonoscopy  Screening at 50yo, or 10 years • Dx: CXR  colonic dilation before dx of relative o • Tx: surgical decompression of colon; may also require Flexible sigmoidoscopy, stool DNA ▪ colostomy or complete colonic resection Tx: o o Management of fluids and electrolyte balance post- Chemoprevention: NSAIDs (ASA), Calcium pills o Lifestyle modification: less fat, more fruit, more fiber surgery o  Surgery: primary tx modality ▪ Colonic resection w/neg. margins, 12+ LNS for examination/staging ▪ Radiation therapy (esp, rectal cancer) o Chemo/combo therapies ▪ Prognosis: incurable metastiatic dz median survival 6mo – 2yrs Pancreas Acute Pancreatitis Chronic Pancreatitis • Etiology ▪ Recurrent episodes of pancreatic inflammation most o Gallstones, chronic ETOH use (2/3 of cases) commonly due to ETOH o ETOH use most common cause in US; gallstones most ▪ Pathophysiology: common cause worldwide o Change in inflammatory environment  shift to o Hypertriglyceridemia, chylomicronemia chronic inflammation  fibrosis and calcification o Hypercalcemia, viruses (mumps, CMV, HSV, HIV, o Self-perpetuating (anxiety/stress can cause more varicella, coxsackie) pain/inflammation leading to more anxiety/stress) o Trauma: blunt, bleeding, retroperitoneal, procedural ▪ Etiologies: (ERCP), malformed ducts, ischemia, vasculitits, SLE o ETOH abuse ▪ Clinical presentation: o Hereditary –autosomal dominant, high risk for o Epigastric pain, frequent radiation to back pancreatic adenocarcinoma o Worse lying supine, with movement o Autoimmune, Hypertriglycerides, 20% no clear cause o N/V, sweating, anxiety, agitation ▪ Lab findings: No elevation  mild elevation o Worse w/ PO intake  NPO w/antiemetics and ▪ Treatment analgesics, ice chips only o Remove offending agent (ETOH cessation) ▪ Lab findings: o Pain control (non-narcotic and narcotic) o Serum lipase and amylase elevation o Pancreatic enzymes: reduces pain by decreases ▪ Elevation does not correlate w/severity amount of work of pancreases o Hgb & Hct (with dehydration Hgb may go up) ▪ Decreases enzymes secreted through neg. o Leukocytosis feedback, Supply w/every meal o BUN/Cr elevation (dehydration), LFTs elevated, Alk o Steroids for autoimmune Phos elevation, triglycerides (over 1000) ▪ Needs to be prescribed by GI specialist; can ▪ Imaging: impair glucose control (difficult to prescribe o Confirms dx, determines etiology, defines prognosis in diabetics) o US – best for evaluating biliary tree o Nerve blocks via EUS to celiac plexus o CT w/contrast – evaluate pancreas for necrosis, ▪ Mixed results, indicated for pts refractory pseudocyst, stranding, r/o other abd etiologies to tx ▪ Stranding – inflammation around pancreas ▪ Prognosis: Difficult condition to manage, no cure ▪ Pseudocyst – mass in pancreas due to inflammation; if infx needs to be drained; Neoplasms/pseudocysts can rupture causing bleeding and ascites; • Typically develop 4+wks after episode of acute pancreatitis not a true cyst (lacks epithelial layer, tends • Due to necrosis or liquidfaction, disruption of pancreatic duct to grow and cause complications) w/leakage o MRI - magnetic resonance cholangopancreatography • Can be seen in chronic pancreatitis, pancreatic trauma (MRCP) used to evaluate stone in CBD • Often asx, abd pain, biliary, obstruction, infx, bleeding ▪ Prognosis  Ranson’s criteria • May resolve spontaneous o 5 markers evaluated at admission • If large/sx  percutaneous/surgical/endoscopic drainage ▪ Age >65, WBC > 15,000, glucose >200, LDH >350, AST >250 Adenocarcinoma o 6 markers evaluated over next 48hrs • 4th leading cause of CA death in US ▪ Hct drop >10%, serum Ca <8%, base • Most common in males and AA’s >45yo, and in the west deficit >4.0, BUN increase >5, fluid • Poor prognosis – overall 5yr survival rate >5% sequestration >6L, arterial PO2 <60 • RF’s: hereditary pancreatitis, lynch syndrome, chronic o Increased mortality w/higher score pancreatitis, tobacco, obesity ▪ 5% mortality risk w/<2signs, 40% • Clinical presentation: abd pain, jaundice, weight loss, mortality risk w/5-6 signs ▪ Tx: anorexia, nausea, back pain, diarrhea, steatorrhea o Remove offending agent and supportive therapy • Dx  biopsy o ▪ IVF, NPO, NG tube if ileus develops, opioid Tumor markers: CA 19-9 (more accurate for larger analgesia, abx if indicated tumors) o o Biliary duct dilation  MRCP, ERCP US  better for larger tumors, CT o o Surgical tx MRI/MRCP – usually better than CT o ▪ Remove gallbladder ERCP  bx and stent placement can occur in same ▪ Placement of percutaneous drain if procedure cholangitis (infx biliary tree) • Tx  Surgery = curative ▪ Debridement of necrotic tissue o Only 15-25% candidates, can’t do it metastatic dz, ▪ Drain pseudocyst malignant ascites, invasion into blood vessels o May use chemo, radiation, combo therapy for pre- operative shrinkage, post-operatively, unresectable tumors Rectum Hemorrhoids Anal abscess • Affect 50% population, M>F • Infection of small anal glands • Varices of hemorrhoidal plexus • Perianal abscess is most common  painful boil-like swelling • RF’s: pregnancy, obesity, long-term sitting, genetics, older age near the anus • Internal Hemorrhoids • Surgical I&D = treatment for all types of anal abscesses o Painless bleeding after defecation • About 50% of abscesses  fistula, can lead to recurrent anal o Visible during anoscopy abscesses o Not palpable or painful on DRE o Surgery is needed to cure almost all anal fistulas o Management  1% hydrocortisone • Etiologies of an abscess o Refer to GI for rubber band ligation if prolapsed o Infection of an anal fistula, STI, blocked anal glands (bulging out of anus) • Risk factors: • External Hemorrhoids o Colitis, IBD (Crohn’s/UC), DM, diverticulitis, PID o Rarely bleed but are extremely painful, especially if o Being the receptive partner in anal sex thrombosed (blueish perianal nodule) o Use of medications such as prednisone o Visible externally on perianal exam o Management  Sitz bath, 1% hydrocortisone Fistula ▪ Stool softeners • Occur due to ulcers, rectal abscesses ▪ May need to remove thrombosed clot • Clinical presentation: o Perirectal/perianal: MC, painful swelling at anus, Proctitis painful defecation  erythema, tenderness • Inflammation of the lining of the rectum (caused by radiation) o Deeper abscesses: buttock/coccyx pain, rectal • Proctitis can cause rectal pain and the continuous sensation fullness  fever more likely that you need to have a bowel movement • Tx: o Surgical drainage, warm-water cleansing, analgesics, Pilonidal cyst stool softeners, high-fiber diet ▪ Infection of skin & subQ tissue at top of intergluteal fold o Fistualectomy ▪ Pilonidal cavity may be asymptomatic ▪ Can become infected and a sinus tract can develop  an Fissures acute subcutaneous abscess develops, spreads along the • Posterior most common tract, and may discharge its contents through a pilonidal sinus • Lateral more pathologic (AIDs, cancer, syphilis, Crohn’s) in the skin cephalad to the natal cleft • Excruciating pain during defecation, assoc. w/ BRBPR ▪ Treatment • Tx: bulking agents, inc. fluids, sitz baths, topical NTG o Abscess → I & D o Recurrent → excise sinus & tracts o Cephalexin, Dicloxacillin, Clinda Fecal impaction • Risk factors  immobility, nervous system dysfunction that damages GI nerves o Medications  Anticholinergics, antidiarrheals, opiates • Symptoms • Common symptoms include: o Abdominal cramping and bloating o Leakage of liquid or sudden episodes of watery diarrhea in someone who has chronic (long-term) constipation o Rectal bleeding, small, semi-formed stools, straining when trying to pass stools • Other possible symptoms include: o Bladder pressure or loss of bladder control, lower back pain o Rapid heartbeat or lightheadedness from straining to pass stool • Dignosis o Hard mass of stool in the rectum o Colonoscopy to screen for cancer • Treatment o Removal of the impacted stool o Warm mineral oil enema is used to soften and lubricate the stool o The mass may have to be broken up by hand. This is called manual removal o Suppositories inserted into the rectum may be given between attempts to help clear the stool o Surgery is rarely needed to treat a fecal impaction o An overly widened colon (megacolon) or complete blockage of the bowel may require emergency removal of the impaction

Celiac Disease Malabsorption syndromes – vitamin/nutritional deficiencies • T-cell mediated gluten intolerance ▪ Global malabsorption results from diseases associated with • Incidence: frequency low (1/3000 persons) either diffuse mucosal involvement or a reduced absorptive • Clinical presentation: weight loss, diarrhea, excess flatus, abd surface. cramps ▪ An example is celiac disease in which diffuse mucosal disease o Rare neurologic symptoms: brain fogs, can lead to impaired absorption of almost all nutrients. anxiety/depression ▪ Classic manifestations: • Diagnosis o Diarrhea with pale, greasy, voluminous, foul- o Serologic markers: IgA anti-tissue transglutaminase smelling stools and weight loss despite adequate test, IgA antiendomysial ab test food intake. o EGD with biopsy = test of choice o However, the majority of patients have relatively ▪ Mucosal intestinal biopsy of distal mild gastrointestinal symptoms: anorexia, flatulence, duodenum or proximal jejunum (will see abdominal distension and borborygmi blunted villi/flat mucosal surface) o Clinical manifestations related to a specific • Treatment  Dietary elimination (wheat, barley, rye) micronutrient deficiency can predominate in some • Complications: patients o Nutrient deficiency (iron, folate, Ca), ▪ Example  iron deficiency anemia or osteopenia/osteoporosis, increased risk of CA (gut osteopenia may be a clue towards celiac lymphoma, non-Hodgkin’s lymphoma X15%), skin disease involvement (dermatitis herpetformis) • Follow up: o Serologic testing 6-8mo after starting gluten free diet (Ab’s should be negative after cessation of ingesting gluten) • Non-celiac gluten sensitivity: no true celiac disese but have sx’s of gluten intolerance; abstain from gluten just as with celiac disease Thiamine deficiency B12 deficiency (Cobalamine) ▪ Thiamine is involved in many cellular metabolic activities and ▪ B12 needed to convert homocysteine to methionine for DNA participates in initiation of nerve impulse propagation. synthesis ▪ Thiamine is found in foods such as yeast, legumes, pork, ▪ Stores last for yrs, absorption occurs in ileum brown rice, and cereals made from whole grains ▪ Etiologies ▪ Thiamine deficiency causes clinical phenotypes of beriberi o Malabsorption  pernicious anemia MC, EtoH, and Wernicke-Korsakoff syndrome Crohn’s, meds (H2RA, PPIs) o Beriberi  has two clinical phenotypes, described as o Decreased intake (found in animal products) "dry" or "wet." Dry beriberi is the development of a ▪ Sx  Pallor, Glossitis, Stomatitis, GI sx, Psych sx, symmetrical peripheral neuropathy characterized by Hyperhomocysteinemia, Neurologic sx’s (peripheral both sensory and motor impairments, mostly of the neuropathy LE, abnormal Babinski) distal extremities. Wet beriberi includes signs of ▪ Dx  Peripheral smear: MCV >115, hyper-segmented cardiac involvement with cardiomegaly, neutrophils, macroovalocytosis cardiomyopathy, heart failure, peripheral edema, o Increased serum homocysteine & methylmalonic and tachycardia, in addition to neuropathy acid (decreased B12 <170 (normal = 240) o Wernicke-Korsakoff syndrome  often associated o Pernicious anemia: (+) ab, parietal with alcoholism but can also occur in other cell ab, inc. levels, (+) Schilling test situations including malabsorption, (poor dietary ▪ Tx  B12 replacement (IM), watch for hypokalemia intake, increased metabolic requirement, and in (reticulocytes produced during tx take up large amounts of K) dialysis patients) ▪ Complications  Spinal cord demyelination & degeneration ▪ Untreated, it leads to coma and death (ataxia, weakness, vibratory, sensory, and perception deficits, ▪ Prognosis is improved by immediate dec. DTR) administration of parenteral thiamine ▪ Thiamine supplementation, along with other multivitamin Folate Deficiency supplementation, is recommended for patients at risk for ▪ Required for DNA synthesis, absorption occurs in jejunum thiamine deficiency ▪ Etiologies  Malabsorption, Pregnancy, Hemolysis (inc. cell turnover deplete folate stores), Meds (MTX, bactrim) ▪ Sx  Pallor, Glossitis, Stomatitis, GI sx, Psych sx, Hyperhomocysteinemia, No neurologic sx’s ▪ Dx  Peripheral smear: MCV > 115, hyper-segmented neutrophils, Decreased folate, Normal B12 ▪ Tx  Folic acid 1mg PO qid ▪ Complications  Fetal neural tube deficits if during