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EsophagusWhat is Esophagitis?Inflammatory changes to the lining of the esophagus (squamous epithelium)Esophagitis Symptoms:DysphagiaChest PainOdynophagiaCauses:GERD (#1)RadiationPillsCaustic IngestionEosinophilic InfiltrationInfectionDiagnostic Tests:Gold Standard: EndoscopyBravo Study: Ambulatory Esophageal pHAgents that can cause esophagitis due to mucosal injury:BisphosphanatesAspirinIron saltsNSAID’sPotassium chloride tabletsQuinidineTetracyclineThere are various scales available to quantify esophagitis severity. The Hetzel-Dent scale utilizes a rating of 0 to 4, with 0?indicating no abnormalities and grade 4 indicating deep peptic ulcerations or confluent erosions involving more than 50% of the mucosal surface of the distal 5 cm of esophageal squamous mucosaInfectious Esophagitis: THINK Immunocompromised!CMV (Chemo/HIV)Ganciclovir (5mg/kg IV q 12 hours x 3-6 weeks)CandidaFluconazole 100mg/d P.O. x 14-21 daysSuspect in patients w/ DM or recent steroid or ABX treatmentHerpeticAcyclovir 400mg 5x daily for 10 daysFamciclovir 500mg BID or Valacyclovir 500mg BID x 10 daysEosinophilic Esophagitis:Affects children to adults 20-40 y.o Males > females (3:1)History of allergies, eczema, asthma or GERD is common“Feline esophagus” on EGDOften causes solid food dysphagia due to esophagitis and dysmotilityCBC w/ diff. reveals eosinophilia – systemic response to something allergicConsider checking tTG for celiac disease and consider food allergy testingTreat acid suppression aggressively with PPI b.i.d. For 6-8 wks and may consider Montelukast (Singulair) 10mg daily or Budesonide susp 1mg B.I.D.Trachealisation – “Feline Esophagus”Achalasia:Idiopathic motility disorder involving loss of peristalsis in the distal 2/3 of smooth muscle and impaired relaxation of LES.Likely the result of neuronal abnormalitiesDysphagia (solids & liquids), Chest Pain, Weight lossAge 25 and greaterAlso consider Scleroderma or late stage Chagas’ disease (South American Trypanosomiasis)Esophageal Varices:Dilated submucosal veins that develop in patients with underlying Portal Hypertension / Cirrhosis and may result in serious upper GI bleeding in 1/3 of patients.Usually occurs in distal 5 cm of esophagusHigher mortality rate than any other source of UGI bleeding.Identified via upper endoscopyActively Bleeding Treatment = ABC’s, page GI or Surgery statManagement:Emergency stabilization (fluids IVs etc)Treat underlying coagulopathy (if present)Endoscopy with banding or injection sclerotherapyBalloon tamponade (if hemorrhage is too vigorous)Mallory-Weiss Tear:Non-penetrating mucosal tear at the GE junction caused by retropulsion of the gastric cardia into the chest during repeated vomiting/retching~ 5% of GI bleedsSmall, fresh hematemesisCommon in young adults or those with history of ETOH abuseDiagnosis is confirmed endoscopically (EGD)Boerhaave’s Syndrome:Caused by a sudden increase in intraesophageal pressure + negative intrathoracic pressure caused by straining or vomiting.Tear most often occurs @ left posterolateral aspect of the distal esophagus and can extend several centimeters.Often associated with alcoholism or hx. of peptic ulcer disease Can lead to MediastinitisSymptoms:History of vomiting or retching followed by acute, severe retrosternal chest and upper abdominal pain.OdynophagiaFeverCyanosisShockGERD:Also known as Pyrosis or old fashioned “heartburn” Refers to backflow of gastric acid and/or duodenal contents (bile acid) into the esophagus and past the LES (lower esophageal sphincter) without associated belching or vomiting. Affects 20% of adults who report at least weekly episodes, 10% of adults report daily heartburn.Risk Factors:ObesityDelayed gastric emptyingPregnancy Systemic sclerosisHiatal herniaRecumbencySmokingAlcohol useMedication such as CCB’s, nitrates, Theophylline Consuming large meals (within 3 hours before bedtime) – one of the main things that will help with nocturnal reflux Wearing tight beltsFoods: chocolate, coffee, peppermint, or fatty food, garlicPathophysiology:Impaired acid neutralization by saliva and HCO3Impaired esophageal motilityLES (inappropriate relaxation)Hiatal herniaDelayed gastric emptying (Gastroparesis)Typical (Esophageal) Clinical Presentation:Heartburn *classic*Bitter taste in the throatAcid regurgitationDysphagiaOdynophagiaWaterbrashAtypical (Supraesophageal) Presentation:Chest painLaryngitis (Hoarseness)AsthmaSinusitisChronic coughAspiration pneumoniaTooth decayRecurrent sore throatFrequent throat clearingGlobus sensationTreatment:Antacids (Tums, Rolaids) neutralize secreted HClH2-receptor antagonists (H2RAs) block the histamine receptor, interfering with one of the stimulation pathwaysProton pump inhibitors (PPIs) block acid at its source in the proton pump of the parietal cell. (1st Line)Omeprazole (Prilosec) 20 mg Lansoprazole (Prevacid) 15 to 30 mgRabeprozole (Aciphex) 20mgPantoprozole (Protonix) 40mgEsomeprazole Magnesium (Nexium) 40mgOmeprazole w/Sodium Bicarb (Zegerid) 40mgDexlansoprazole (Dexilant) 60mgSide Effects of PPI’s: HA, diarrhea, nauseaProkinetic drugs (Zelnorm, Reglan)Antireflux surgery (Nissen Fundoplication)Esophagitis secondary to GERD:Severe Reflux from GERD (incompetent LES) can lead to esophagitis. Diagnostic Histology:Intraepithelial EosinophilsThe severity of symptoms is not related to the degree of histologic esophagitisConsequences: bleeding, stricture, Barrett esophagusTreatment: Lifestyle modification elevate head of bed, no bedtime snacksno smoking/alcoholdecrease meal size and fat intakeavoid caffeine (chocolate, coffee, tea, cola) peppermint, citrus fruitMedications – antacids, H2 receptor blockers, proton pump inhibitorsBarrett’s Esophagus:A self-protective mechanism by which squamous epithelium in the distal esophagus is replaced by columnar epithelium (gastric).3 types of gastric columnar epithelium, **Intestinal metaplasia is the type that increases the risk of adenocarcinoma.Secondary to chronic reflux-induced injury – compensation by the body but this causes a lot of cellular turnover Affects ~ 10,000 people per year in U.S. 5 year survival rate < 15% if you have adenocarcinoma Pay attention to GERD complaints in old, white males with truncal obesity. (Sutton’s Law)“Tongue” of Barrett’sTreatment:long-term PPI therapy and adherence to anti-reflux measuresAdvised to have repeat endoscopic surveillance at 2 to 3 year intervalsIncidence of Barrett’s evolving into esophageal adenocarcinoma is 2 in 200.Squamous Cell Esophageal Cancer:Blacks > whitesMost prevalent worldwideAssociated with:ETOHTobacco abuseHuman Papilloma Virus> 50% involve distal third of esophagusOverall 5- year survival rate is < 15% for either form of Esophageal CancerMore Nodular:Adenocarcinoma Esophageal Cancer:Prominent in whitesIncidence risingAssociated with ObesityMost cases arise from Barrett’s changes and chronic GERDInvolves distal third of esophagusOverall 5- year survival rate is < 15% for either form of Esophageal CancerMore Spread out:Esophageal Web:A thin, diaphragm-like membrane of squamous mucosaMid to upper esophagusMay be multipleCongenital or may be related to Plummer – Vinson SyndromePlummer-Vinson Syndrome:Predominately in CaucasiansFemale > male; 40-70 years oldPredominant findings are dysphagia with a history of iron-deficiency anemia.Esophageal “Schatzki Rings” Smooth, circumferential and thin mucosal structures found at the GE junction (distal).Lead to dysphagiaStrongly associated with Hiatal HerniasSuspected secondary to GERDTreatment = Esophageal DilationEsophageal Strictures:Most found in mid to distal esophagusMajority result from chronic inflammation and GERDUsually benign Can be associated with Barrett’s EsophagusMay also be caused by burns Pills that got stuck and disintegrated the tissueTreatment: Esophageal Dilation Balloon Method:Maloney-Dilator Method:Zenker’s Diverticulum:Protrusion of pharyngeal mucosa @ PE junction (posterior protrusion most common).Caused by loss of elasticity of UESUsually older patientsSymptoms:HalitosisDysphagiaNocturnal ChokingDiagnosis: Barium SwallowTx: SurgeryBenign Esophageal Tumor: LeiomyomaThe most commonSubmucosal, nodular lesionsMost are asymptomatic, although larger lesions can cause dysphagia. Endoscopic ultrasonography** is test of choice because endoscopic biopsies are generallyStomachPeptic Ulcer Disease:Include both Gastric and Duodenal ulcers~ 10% of adults develop PUD in their lifetimeEpigastric Pain (dyspepsia) often described as gnawing, dull, “hunger-like” discomfort.Most common cause of Upper GI bleedingDuodenal Ulcers 5x more common, younger patientsPain relieved with food or antacids, recurs 2-4 hours after a meal, or a strong nocturnal componentGastric Ulcers more common in ages 55-70 , high association with cancerPain aggravated by food and associated with weight loss and “fear of eating”Associated symptoms: Nausea, Anorexia, Abdominal bloating, vomiting, melena, weight loss, hematemesis(3) major causes :NSAIDS – inhibit prostaglandin synthesis. Prostaglandins are known to increase mucosal blood flow, increase bicarb and mucous secretion and stimulate mucosal repair. Aspirin is the most ulcerogenic NSAID (beware of BC, Goody’s powders and Alka-seltzer).H. pylori – gram neg. bacillus that resides in the mucous gel coating the epithelial cells of the stomach. Suspected to cause a defect in protective barrier that can then lead to chronic gastritis and ulcer formation.Zollinger-Ellison (ZE) syndrome – benign gastrin-secreting tumor usually located in the pancreas or duodenal wall that results in uninhibited secretion of gastrin (Hypersecretion) and constant acid production. Leads to development of peptic ulcers in 90% of patients; diarrhea is common. < 1% of PUD is caused by ZE syndrome, may be associated with MEN type 1Complications: PerforationDiagnosis:Upper Endoscopy with biopsy is diagnostic test of choice.CBC, BUN if suspected GI bleeding.H.pylori serology gives limited information for active involvement of H.pylori. Need gastric biopsy to confirm active infection.Consider checking a fasting serum Gastrin level if peptic disease is persistent (to r/o ZES). Need to stop PPI therapy before testing.Management:Pharmacotherapy is directed at reduction of acid secretion, preserving mucosal defenses, and eradication of H.pylori infection.Proton pump inhibitors are currently the treatment of choice for PUD, given their high safety and efficacy bination antibiotic regimens with PPI are most effective in eradicating H.pylori.Regular, well balanced diets with elimination of caffeine, sodas, acidic foods, NSAID’s, ETOH and smoking.Gastritis:superficial inflammation and erosions of gastric mucosa without penetration into the submucosa or muscularis.Patients are usually asymptomatic but can progress to dyspepsia, anorexia, nausea and vomiting.Accounts for < 5% of GI bleeds.Acute Gastritis:NSAIDs Biphosphonates PotassiumMacrolides ETOHStressVirusesBacteriaChronic Gastritis:Helicobacter pyloriAutoimmuneLymphocyticBile RefluxEosinophilicCommonly associated with:NSAID’sProlonged stress (physiologic) due to severe medical or surgical illnessHeavy ETOH consumptionCaffeine abuse, and H.pylori.** Psychological StressDiagnosis:Endoscopy with biopsies for H.pylori.Treatment:Proton Pump inhibitors and cessation of offending medication, ETOH, or caffeine.Gastric Cancer:Most neoplasms of the stomach are malignant and most of those are adenocarcinoma.Adenocarcinoma of the stomach is the 2nd most frequent cause of cancer world-wide.Incidence has declined in Westernized countries; attributable to improved diet and refrigeration (has eliminated the need for salting, smoking, preserved foods.) Risk Factors:Chronic Gastritis w/ H.pyloriNational origin (Japan, Chile, Finland)Diet (high sodium/nitrates)Blood group AMale>FemaleHx of partial gastrectomyFamily hx of gastric cancer autosomal dominantSymptoms:Early typically asymptomaticAbdominal PainWeight loss/anorexiaGeneralized weaknessGI bleedingEarly satietyPhysical Exam:Epigastric massEnlarged massAscitesPelvic mass if gastric cancer has mets to the ovaries (Krukenberg tumor)Diagnostic Studies:EndoscopyUpper GI seriesCEA level – elevated in 1/3 of patientsCBC (Hgb / Hct) CT abdomen to evaluate for metastasisPrognosis:Poor. 5 year survival 10%Sx is primary hope for curePyloric Stenosis:Hypertrophy of the pyloric muscleAffects infants around 4-6 weeks of ageMost common in first born children5:1 male predominance Presentation:Projectile vomiting after feeding, otherwise not illVigorous/HungryNon-bilious vomitingAbdominal SwellingWeight lossMetabolic Alkalosis due to loss of hydrochloric acidPhysical Exam:“Olive” of hypertrophied muscleReverse PeristalsisDiagnostic Tests:Elevated BUN d/t dehydrationUnconjugated hyperbilirubinemiaPlain films showing gastric enlargement and little gas in bowelsU/S is the study of choice which reveals elongation and thickening of pylorus:Barium Upper GI study reveals a “string sign”:Treatment:Correct fluid and electrolyte abnormalitiesKeep NPOSurgery (pyloromyotomy)Small IntestineSmall Bowel Neoplasms:Overall very rare, <5% of GI cancersOccur in most people >50 years of ageAdenocarcinomas, Lymphomas, Carcinoid tumorsComplications with Increased risk of SB cancers:Crohn’s: adenocarcinomaFamilial adenomatous polyposis: peri-ampullary adenocarcinoma (200fold inc)Celiac sprue: lymphoma and adenocarcinomaAIDS: non-hodgkin’s lymphoma and kaposi’s sarcomaNeurofibromatosis: leiomyopma and adenocarcinomaMelanoma: highest rate of mets to SBSmall Bowel Adenocarcinoma:Most common malignant SB tumorMost often located in duodenum/proximal jejunumAmpulla of Vater m/c site80% of cases have already metastasized by the time of dx. SB surgical resection is recommended for control of sxFindings: anemia/GI bleed, Jaundice, SB obstruction, weight lossSmall Bowel Lymphomas:Most common in distal SBMajority are non-hodgkin’s intermediate or high grade B cell lymphoma’sFindings: Abdominal pain, N/V, anemia, weight loss, abdominal distention, positive hemoccultWork-up: CT enterography, or SBFTTreatment: resection, chemo/radiation – dependent on stage of disease (overall poor prognosis of 20% at 5 yrs)Small Bowel Carcinoid Tumors:Most common neuroendocrine tumors from GI tractSlowest growing, majority are asymptomatic and found incidentallyMay contain serotonin, somatostatin or gastrinCommonly arise in ileumSlow spread but >2cm mass = mets (onset to death is ~9yrs)Findings: abd pain, signs of obstruction, rectal bleeding, change in bowel habits**Carcinoid Syndrome: <10% of pts, caused by tumor secretion of hormonal mediators, may lead to flushing, head/neck edema, bronchospasms, diarrhea, cardiac (valvular) diseaseWork-Up: Plasma Chromagranin A m/c screening test, 24 hour urine for 5-HIAA, abd CT scan, Octreotide scanTreatment: surgeryIf Carcinoid: consider resection of hepatic mets and start octreotide 100-500mcg SC TIDAppendicitis:Most common surgical emergency Mostly between ages 10-30If untreated gangrene and perf within 36 hoursFindings:Initially vague periumbilical abdominal pain that later locates to the RLQAnorexiaNausea / vomiting+/- fever+/- leukocytosisTenderness over McBurney’s Pt.Positive bounce testAids to Diagnosis:H&PCBCSerum PregnancyUACT abd/pelvisMake NPO and consult surgery!**Be aware of retrocecal appendix!Irritable Bowel Syndrome:Constipation, diarrhea, or alternating with bothAbdominal painBloating/distentionMucous in stoolSx related to stressWeight stableMust be present at least 3days/month for longer than 3 monthsFemales > MalesAges 18-45 most commonFood is the most common culprit (up to 2/3 of pts associate sx with eating a meal)Clinical Work-Up:Stool for occult bloodIf diarrhea: stool for O&P, C&SColonoscopyConsider labs for tTG, CMP, TSH, CBCTreatment:Reassurance and EducationStress reductionRegular exercise and diet modificationConsider use of TCA’s or SSRI’sIncrease soluble fibers, H2OStool Softeners, Laxatives, Lubiprostone or antidiarrhealsMAINSTAY: Psyllium husk powder (Metamucil)**Alarm Symptoms: weight loss and rectal bleeding refer to GI Large IntestineDiverticular Disease:Very common in westernized countries where dietary fiber has been replaced by refined carbsPrevalence increases with ageMost will remain asymptomatic Caused by increased intra-luminal pressures over time small herniation of the colon wall Most are found in the sigmoid colon (smaller radius)Diverticulitis Symptoms:LLQ abdominal painChange in bowel habits (constipation- 50%, diarrhea 25%)Rectal bleedingFever, ChillsNausea and VomitingDiagnosis:CBC, CMP, UA, Serum pregnancyCT abd/pelvis (if fever or 1st episode), DRELeukocytosis is mc lab findingColonoscopy contraindicated within 6-8 wks of infection due to inc risk of perforationTreatment:Bowel rest, NPOCiprofloxacin + Metronidazole or Augmentin (2nd line)Gradually increase fiber and maintain high fiber dietSurgery may be considered for severe segments of diverticulosisComplications: bleeding, abscess, perforationInflammatory Bowel Disease:Crohn’s + Ulcerative Colitis1/3 of cases present in 2nd decade of life and between the 6th and 7th decadesPotential risk factors:Family history *most importantHigh level of sanitation (CD)Cigarette Smoking (+ CD, -UC)Increased sugar intake, esp CDSigns & Symptoms of Crohn’s:Non bloody diarrheaAbdominal pain (RLQ)Anorexia/Weight lossPeri-anal abscess, fistula, chronic fissureGrowth retardation in childrenN/V, feverErythema nodosumArthralgiasApthous stomatitisSigns & Symptoms of UC:Bloody diarrhea with mucusTenesmusFecal incontinenceAbdominal Pain + TendernessFeverm fatigue, loss of appetite/weightArthralgiasUveitisSkin UlcersJaundice (with primary biliary cirrhosis)IBD Complications:Crohn’s: fistulas, abscess, intestinal blockage, extraintestinal disorders, malnutrition, colon or rectal cancer, growth retardationUC: severe inflammation, perforation, megacolon, extraintestinal disorders, colon or rectal cancerWork-Up for Crohn’s:CBC: anemia, iron def, B12 malabsorptionCMP: hypoalbuminemiaESR/CRP: elevatedIBD panel: autoantibodiesStool Studies: C&S, O&P, Fecal fatColonoscopy: to evaluate/biopsySmall bowel radiographsTreatment for Crohn’s:SurgeryNatalizumab (anti-TNF)Prednisone, 6-MP, AZA/MTX, Budesonide, ABX, AminosalicylatesTreatment for Ulcerative Colitis:Surgery: ColectomyBiologics: Cyclosporine, infliximabCorticosteroids: Steroids (short term), Azathiprine/6MP (long term)Aminosalicylates: 5-ASA’s (mesalamine)Colorectal Cancer:Third mc type of cancer and cause of cancer-related deathMost colon cancers arise from pre-existing polypsMean age at dx: 64Risk Factors:Age (>50)Prior hx of adenoma or carcinomaFamily hx of CRCIBDHigh fat/low fiber consumptionBeer and ale consumptionHereditary Colorectal Cancers:Familial Adenomatous Polyposis (FAP): APC geneHereditary non-polyposis colorectal cancer (HNPCC): MMR genesScreening:Colonoscopy: Gold Standard q10yearsFlexible sigmoidoscopy q5yrsDouble contrast barium enema q5yrsCT colonography q5yrsFOBT qyearColon Polyps:Mucosal neoplastic (adenomatous) tubular, villous, tubulovillous, seratedMucosal non-neoplastic (hyperplastic) hyperplastic, juvenile, inflammatorySubmucosal lesions lipomas, lymphoid aggregatesRemove via colonoscopyPancreasAcute Pancreatitis:May be related to edema or obstruction of ampulla, reflux of bile, direct injury to acinar cells, biliary tract dz, cyst, abscess, pancreas necrosisMost common causes in US: Biliary Tract disease and/or ETOHABRUPT onset of deep epigastric pain possibly associated with radiation to the back and worse when lying downPain improved when leaning forwardHistory of prior episodes (usually involve alcohol or consumption of a heavy/greasy meal before attack)Symptoms:Steady/boring/severe epigastric painN/VDiaphoresis, weaknessHypotension, pallor, clammy skinPhysical Exam:Tender epigastric region, +/- guarding/rebound/rigidity, abdominal distention, dec bowel soundsCullens sign or Grey Turner’s sign if severe necrotizing pancreatitis with hemoperitoneumComplications:ARDS (usually 3-7d after fluids)Pancreatic necrosisPancreatic pseudo cystPancreatic cyst or abscess**Necrotizing Pancreatitis in 5-10% of cases and accounts for mst deathsRanson Criteria on AdmissionAge greater than 55 yearsWBC greater than 16,000/ulBlood glucose greater than 200 mg/dlSerum LDH greater than 350 I.U./LSGOT (AST) greater than 250 I.U./LRanson Criteria in first 48 hoursHematocrit fall greater than 10%BUN increase greater than 8 mg/dlSerum calcium less than 8 mg/dlArterial oxygen saturation less than 60 mm HgBase deficit greater than 4 meq/LEstimated fluid sequestration greater than 6000 ml (6 liters) Ranson score of 0-2, minimal mortalityRanson score of 3-5, 10%-20% mortalityRanson score of >5 has more than 50% mortality and is associated with more systemic complications.Lab Testing:Increased amylase and lipase (3x normal) – lipase remains elevated for a week, amylase for 72hoursLeukocytosisHypocalcemiaProteinuriaHyperglycemiaFasting TG >1000mg/dL** Hct>44% or inc Serum Cr, worry about pancreatic necrosisRise of ALT may mean biliary pancreatitisImaging:Plain radiographs for setinal loop, gall stones or colon cutoff signAbd ultrasound for gallstonesnoncontrastCT ABD test of choiceMRCP for repeated attacksTreatment:Most resolve without tx (supportive)NPO (bowel rest) & Bed restNG tube if neededIV crystalloid resuscitation (250-300 mL/hour for the first 48hrs)Pain meds: Meperidine or MorphineLap Chole if biliary pancreatitisSevere Treatment:Supportive measures +:Vigorous fluid resuscitation and check HCT q12h (if decrease then hydration is adequate)TPN for7-10dAbx if necrosis (imipenum 500mg IV q8h x 14d)If abscess surgical drainageChronic Pancreatitis:Prolonged inflammatory, fibrosis of the organ70-80% associated with alcoholism Tobacco accelerates progressionUsually develops in 5-10% of alcoholicsHallmark features = abd pain (chronic epigastric or LUQ pain that radiates to the back and is unrelenting) and pancreatic insufficiency (steatorrhea- late finding with weight loss)TIGAR-O: classification of chronic pancreatitis etiology:Toxic Metabolic: alcohol, tobacco, hypercalcemia, chronic renal failureIdiopathicGenetic: Autosomal DominantAutoimmune: Sjrogen, primary sclerosing cholangitis, Type1DM, primary biliary cirrhosisRecurrent: post necrotic, vascular/ischemiaObstructive: pancreas divisum, duct obstruction from tumors or post traumaLab Testing:Increases in Amylase/Lipase – remember that the longer the abuse or deterioration of the pancreas, the more the labs will appear normal.Alkaline phosphataseTotal bilirubin -- Elevation of liver function tests may signal compression of the pancreatic portion of the bile duct by edema, fibrosis, or tumor development.Sudan stain to confirm fecal fat excretionFecal Pancreatic Elastase (FPE-1) -- An ELISA stool test that serves as a marker of exocrine pancreatic function (<100)Imaging:Plain films show calcificationsCT/MRI – mainstayMRCP (noninvasive)ERCP (invasive)Treatment:Low fat dietAlcohol abstinenceSmoking cessationAnalgesics (avoid narcotics if possible)Pancreatic supplements (Creon, Pancrease)- Allows them to digest betterAutoimmune- Corticosteroids (Prednisone taper)Treat diabetes if indicatedSurgical Options:Drain pseudocystsRelieve biliary obstructionsRule out pancreatic CAERCP- ductal dilitation/stentComplications:Opioid addictionPancreatic CA develops in 4% after 20 years of condition>80% develop diabetes (25 years after onset)Others: pseudocyst, fistula formation, pseudoaneurysm, CBD stenosis, splenic/portal obstructionPancreatic Cancer:2% of all cancers (5% of all CA deaths)7-8% have familial relation of CA95% of all CA arises from exocrine portion of pancreas75% are in the head, 25% in body and tail (pain in RUQ)Mean survival 11.2 months- dependent on stagingMore common in menMore in African Americans, Polynesians and native New ZealandersRare before age 45 , but increases sharply after the 7th decade. Types:Ductal Adenocarcinoma (most common – 90%) –arise from epithelial cells in the exocrine ductsNeuroendocrine tumors aka carcinoidCystic neoplasm if cyst and no history of pancreatitisRisk Factors:AgeObesityTobacco use (thought to cause 20-25% of cases)Chronic pancreatitisPrior abdominal radiationFamily HistorySymptoms:Obstructive painless jaundice (if pancreatic head) ddx is duodenal cancer, ductal carcinoma, Enlarged gallbladder (+/- pain)Upper abdominal pain or discomfort described as vague and diffuse pain (gnawing pain)Weight loss/ AnorexiaDiarrheaNew onset DMThrombophlebitis (late stage)Sister Mary Joseph’s nodule- hard, palpable nodule that bulges from the umbilicus. (Results from abdominal or pelvic metastasis)Courvoisier sign: a palpable, non tender gall bladder due to the CBD becoming obstructed by a pancreatic neoplasmLaboratory Testing:Most labs normal (if cancer is in the tail)Elevated glucose in 10-20% casesCA 19-9: not sensitive for early detection but can be useful in diagnosis and monitoring treatmentAlk Phos 4-5x elevatedBilirubin elevatedHepatic Transaminases (AST/ALT) elevatedAmylase/Lipase elevatedImaging:Spiral CT *BestMRI as an alternativeEndoscopic USERCPTreatment:If duodenal obstruction- gastrojejunostomyChemotherapy has a high resistance and is not very effective, alone or with radiationRadiation alone has little impact15-20% present with disease that can be resected, local invasion determines successThe Whipple Procedure: pancreaticoduodenectomyPrognosis:5 year survival with no treatment 2-5%20-40% if resectableIf family history present, recommend endoscopic U/S and/or CT ABD starting at age 40-45 or 10 years before age at which family member was diagnosed.RectumAnorectal Abscess: A localized inflammatory process that can be associated with infections of soft tissue and anal glands based on anatomic location. Most are located in the posterior rectal wall but can communicate around the rectum (Horseshoe abscess)Presentation:Males> FemalesPerirectal cellulitis or erythemaPerirectal mass by inspection or palpationLocalized perirectal or anal pain often worsened with movement or strainingFever and signs of sepsis with deep abscessUrinary retentionCauses by infection of mucous secreting anal glands:Staph aureusE. coliBacteroides, ProteusStreptooccusDiagnosis: Many people will have predisposing underlying conditions including:Malignancy/LeukemiaImmune deficiencyDM (check BS!)Recent surgery or Steroid therapyWorkup: Rule out necrotic process and crepitance suggesting deep tissue involvementLocal aerobic/anaerobic cultureBlood cultures if toxic/febrile/compromisedPossible sigmoidoscopyImaging studies not indicated unless extensive disease abscessTreatment:I&D of abscess (cures in 50% of cases)Debridement of necrotic tissueChronic recurrence leads to fistula formation fistulectomyLocal wound care/packingSitz bathComplications: Necrotizing fasciitis, sepsis, deathOutpatient Antibiotics:Amoxicillin/Clavulanic acid 875/1000 mg BIDCiprofloxacin 750mg BID+ Metronidazole 500-750mg TIDClindamycin 150-300mg TIDInpatient Antibiotics:Ampicillin/sulbactam (Unasyn) 1-2gm IV q6-8hrsCefotetan 1-2gm IV q8hPiperacillin/Tazobactam 3.375gm IV q6-8hImipenem 500-1000mg IV q8h*According to Kirby: Abx are of unproven value but should be used in diabetics, immunocompromised, sepsis, or those with prosthesis or valvular heart dz.Anal Fissure:A fissure is a tear in the epithelial lining of the anal canal.Men>WomenCommon in women before/after childbirthCan occur at any ageMost common cause of rectal bleeding in infants90% posterior, 10% anteriorAcute anal fissure sx:Sharp burning/tearing pain associated with bowel movementsBRB on toilet paper or streak of blood on the stoolChronic anal fissure sx:Pruritis aniPain seldom presentIntermittent bleedingSentinel tag at caudal aspect of fissure and hypertrophied anal papilla at proximal endUnderlying disease possible if:Ectopically locatedBroad based/deep/purulentExtends proximal to dentate lineEtiology:Large, hard stool passageFrequent defecation/diarrheaBacterial infection: TB, syphilis, gonorrhea, chancroid, lyphogranuloma venereumViral: HSV, CMV, HIVIBDTraumaMalignancy: Kaposis, lymphoma, carcinomaTreatment:Sitz Bath, High fiber diet, inc fluid intake.Bulk producing agent (Metamucil)Stool softeners (Colace, surfak)Local anesthetic jellyNitroglycerin ointmentSurgery (lateral sphincterotomy)Injection of botulinum toxin if chronic. BEWARE:Crohns, anal TB, anal carcinoma, can all present as ulcers so biopsy all chronic ulcersAnorectal Fistula:Chronic form of anorectal abscessA fistula is an inflammatory tract with a secondary (external) opening in the perianal skin and a primary (internal) opening in the anal canal at the dentate line.May be initial sign of Crohn’s, TB, NeoplasmManaged by opening the fistula tract (fistulotomy) and curetting the tract and allowing it to heal by secondary intention.Symptoms:Acute stage: perianal swelling, pain, feverChronic stage: history of rectal drainage or bleeding, previous abscess with drainage.Etiology:Most common: nonspecific cryptoglandular infection (skin or intestinal flora)Fistulas more common when intestinal microorganisms are cultured from the anorectal abscessTB, Lymphogranuloma venereum, actinomycosisIBDTrauma: sx, FB, intercourseMalignancy: carcinoma, leukemia, lymphomaWork-Up:DRE to assess sphincter tone Determine the presence of an extraluminal massIdentify an indurated trackPalpate an internal opening or pitAnoscopyProctosigmoidoscopy to exclude inflammatory/neoplastic dzLabs:CBCRectal Biopsy if IBD/malignancy suspectedImaging:Colonoscopy or barium enema if dx of IBD/malignancy suspected, patient <25, history of recurrent fistulasTreatment:Sitz bathSurgeryBroad-spectrum abx if cellulitis, immunocompromised, valvular heart disease, prosthesisStool softener/laxative***HIV/Diabetic pts with fistulas are true surgical emergenciesRisk of septicemia, fournier’s gangreneHemorrhoids:Valscular and connective tissueUsually located in 3 positions: R. anterolateral, posterior/lateral, left lateralInternal are above the dentate line (painless)External are under the anoderm (same sensation as skin and thus, painful)Grading System: BleedBleed + Prolapse, but spontaneously reducesBleed + prolapse and needs manual reduction IncarceratesExternal Symptoms: pain, pruritis, fullness sensation, thrombosis, +/- bleedingInternal Symptoms: Bleeding (painless)Causes:Lack of soluble fiber, water, strainingIncreased intra-abdominal pressure from pregnancy, obesity, sitting, coughing, sneezing etc.Excessive cleaning, rubbing, steroids or hemorrhoid creamsTreatment:After confirmation via sigmoidoscopy/colonoscopy..High fiber dietStool softenersAvoid heavy lifting/strainingWarm baths BIDMedication for anorectal inflammationAnusol-HC suppositoriesAnalpram or procto-foamW.A.S.H regimen: Warm water, Analgesics, Stool softeners, high fiber dietIf symptoms persist, consider surgical referral.Rectal Neoplasm:AdenocarcinomaTreatment: local excisionlow anterior resection (tumors above 8-10 cm from anus)Abdominal-perineal resectionAnal Neoplasm:Squamous cell carcinomaTreatment:Chemo radiation with 5-FU and Mitomycin or external beam radiationMelanomaTreatment: Wide excisionDiarrhea:Rotavirus:Severe in children between 3 and 15 mos.Shed by feces, transmitted via fecal / oral routeMost common in winter monthsIncubation period of 1 – 3 days. Symptoms last 5 – 7 days.Sx’s = vomiting, fever, watery diarrhea, dehydrationDx = Rotozyme test (viral assay)Tx = symptomatic / supportive with oral or IV rehydrationEnteric Adenovirus:Transmitted from person to personNosocomial outbreaks do occur, but spread to adults in uncommonYear round occurrenceIncubation period = 8 -10 days, lasts 1 – 2 weeksSymptoms: low grade fever, watery diarrhea, then brief vomitingDx: can detect virus on electron microscopyTx: SupportiveClostridium botulinum:Associated with improperly prepared home-canned fruits and vegetables.Responsible for 1/3 of all deaths from food borne illness.Dx: made by history and cultureTX: Golytely bowel lavageClostridium perfringens:Found in soil and GI tract of humans and animalsBeef or poultry sourceRequires inadequate initial preparation and then reheatedSymptoms: watery diarrhea with severe, Crampy pain w/in 8-24 hrs of ingestionDX: historyTX: SupportiveNorwalk Viruses:Year round occurrenceAffects older children and adults (usually not young children)Spreads rapidly via fecal / oral routeMay also be airborne via droplets from vomitus or contaminated laundry.Incubation period = 12 – 48 hoursSymptoms : rapid onset of abdominal cramping, vomiting, diarrheaDiagnosis : H&PTreatment : SupportiveVibrio parahaemolyticus:Gram (-) bacillus that survives in water with high salt content.More common in summerFound in contaminated fish or shellfish (raw or cooked)Incubation = 12 – 24 hoursSymptoms: explosive, watery diarrhea. Headaches, vomitingResolves in 1 – 7 daysDX: stool cultureTX: supportive, if severe consider tetracyclineEnterotoxigenic E. coli:Found in contaminated water or foodSpread via fecal / oral routeMost common travelers’ pathogenRequires large inoculum for disease to emergeIncubation period = 1 to 3 daysSymptoms = abrupt, profuse, large volume diarrhea (like cholera)DX: HistoryTX: supportive, if severe, consider Cipro or Tetracycline.Vibrio Cholerae:Gram negativeContaminated saltwater crabs and freshwater shrimpIncubation period = 1 – 3 daysSymptoms: abrupt onset of PROFUSE, large-volume watery diarrhea. No fever, vomitingBeware of rapid dehydration !!!!Dx: dark field microscopyTx: Volume replacement, may respond to DoxycyclineStaphylococcus aureus:Most frequent cause of toxin-mediated vomiting and diarrheaTransmitted via hands of food handlersProblematic foods: Cole slaw, potato salad, salad dressings, milk products, and cream pastriesSymptoms: Abrupt onset of vomiting within 2 – 6 hrs of ingestion and explosive diarrhea with some abdominal cramping but no fever.Dx = HistoryTx = Supportive, symptoms normally dissipate within 24 hours. Bacillus cereus:Gram +, spore-forming organism found in soilSpores can survive extreme tempsContamination occurs before cookingNormally found in contaminated rice or meat from Asian restaurants.“emesis syndrome” – severe vomiting within 2 – 6 hoursor “diarrhea syndrome” – foul-smelling, profuse diarrhea 8 -16 hrs after eatingDx: historyTx: SupportiveInfectious Diarrhea: CCSSY +EVECampylobacter jejuniC.jejuni is the most common bacterial pathogen that causes bloody diarrhea in the U.S.Transmitted to humans from contaminated pork, lamb, beef, milk products, water, or exposure to infected household pets.Incubation period 1 to 7 daysSymptoms start with malaise, HA, followed by severe abdominal pain, fever and bloody diarrhea.Can lead to systemic infectionDX: made by stool culturesTX: Emycin or CiproSalmonella:Transmitted from fecally contaminated foods and waterPoultry products most commonFever & bacteremia < 10% casesCarrier state can exist, as some patients carry bacteria in GB or in urinary tract. DX: history and + blood/stool cx’sTX: supportive in most cases** Antibiotics contraindicated in most pts b/c it can increase the carrier state. Consider Amoxil, Bactrim DS or Cipro in immunosuppressed adults, pediatric or adults > 65. Shigella:Seasonal preference for winter.Fecal / oral routeCommon in dairy and egg saladCommon in children 6 mos to 5 yrIncubation period 1 to 3 daysDx: stool cultureTx: supportive & AntibioticsBactrim DS, Cipro, TetracyclineDo not use Immodium or Lomotil Enterohemorrhagic E.coli:E.coli 157:07Infection occurs if meat is undercooked.Outbreaks in schools, daycare centers, nursing homesFecal / oral spreadLasts 7 to 10 daysMay be complicated by hemolytic uremia syndromeDX: stool cultureTX: supportive & Cipro antibioticYersinia enterocolitica:Found in stream or lake waters and has been isolated in many animals.Transmitted via contaminated water or from human or animal carriers.Most common in childrenSymptoms = bloody diarrhea, fever and abdominal painDX: stool and blood culturesTX: Supportive, may use Bactrim or Tetracycline for severe illness.Clostridium difficile:Most commonly affects elderly.Spread by fecal / oral transmission or by contaminated hands of healthcare workers Follows antibiotic use, especially: ampicillin, amoxicillin, cephalosporins, clindamycin and fluoroquinolonesSymptoms usually start within 1 week of antibiotic exposure but can range from day one to 10 weeks post antibiotic exposure. (always inquire about any abx use in the past 2-3 mos) Dx: Stool cultures for C.diff toxin (PCR, EIA) **always order x 3Treatment:Stop all offending antibiotics firstReplace fluids/electrolytes (if needed)Avoid anti-peristaltic agents Flagyl (metronidazole) 500mg P.O. TID x 10-14 daysVancomycin 125mg P.O. QID x 10 daysComplications:Pseudomembranous colitisToxic megacolonPerforations **SepsisRecurrent diarrheaNutritional DisordersObesity:BMI >30Increased abdominal circumference (>40 inches (men) and 35 inches (women): Increased risk of DM, HTN, early deathBMIs > 40, cancer risk is 52% higher (men), 62% (women)Etiology:Excess caloric intake and sedentary lifestyleGenetic influencesMetabolic Syndrome:Elevated abdominal Circumference: >40 inches (men) and >35 inches (women)Triglycerides > 150 mg/dLHDL < 40 mg/dL (men), < 50 mg/dL (women)BP > 130/85FBS > 100 mg/dLTreatment:Lifestyle modification: calories, exercise, behavior therapyPharmacotherapy short termSurgery: refer if BMI>40 or >35+ additional health related risksAnorexia Nervosa:Weight loss leading to body weight < 15% below expectedIn females, absence of three consecutive menstrual cycles90% femaleSigns/Symptoms:Emaciation, cold intolerance, constipation, bradycardia, hypotension, hypothermiaAmenorrhea: almost always presentPE: loss of body fat, dry, scaly skin, increased lanugo body hair.Labs:AnemiaElectrolyte AbnormalitiesInc BUN/CrTreatment:behavioral therapy, psychotherapy, family therapy, antidepressantsRefer for psych evalBulimia:Uncontrolled episodes of binge eating at least twice weekly for 3 monthsPrevention of weight gain by self-induced vomiting, laxatives, diuretics, excessive exerciseGastric dilatation, pancreatitis, poor dentition, pharyngitis, aspiration, electrolyte abnormalitiesTreatment:Psychotherapy: behavioral, family, individual, group?antidepressantsVitamin DeficienciesVitamin B1 (Thiamine)Found in cereals, beans, pork, yeast, rice In US, seen with chronic alcoholismEarly Findings:AnorexiaMuscle crampsParesthesiasIrritabilityAdvanced Findings Dry Beriberi: Low calorie intake and inactivity with nervous system involvementPeripheral involvement: both motor and sensory-(symmetric): pain, paresthesias, loss reflexes, Lower>upper extremitiesCentral involvement: Wernicke-Korsakoff SyndromeWernicke encephalopathy: nystagmus progressing to opthalomoplegia, confusion, truncal ataxiaKorsakoff Syndrome: Confabulation, amnesia, impaired learningAdvanced Findings: Wet Beriberi:Very high activity levels and eating large amounts of carbohydratesCardiovascular involvement (high output failure), vasodilatation, dyspnea, cardiomegaly, pulmonary and peripheral edemaDiagnosis:Most commonly used lab test is to measure the erythrocyte transketolase activity (ETKA) and urinary thiamine excretionTreatment:50-100 mg/day IV for several days then po, 5-10 mg/day50% complete resolution within several daysVitamin B2 (Riboflavin)Milk, dairy products, cereals, meats, and dark green vegetablesRarely an isolated deficiency, usually occurs with other Vitamin B complex deficienciesAlcoholism, Malasorption, Celiac sprue Medication interactionsProtein-calorie undernutritionPhysical Exam Findings:Cheilosis/Angular stomatitisGlossitisSeborrheic dermatitisWeaknessCorneal vascularizationAnemiaDiagnosis:Measurement of the riboflavin-dependent enzyme erythrocyte glutathione reductaseMeasure the urinary excretion of riboflavinTreatment:Oral Preparation: 5-15 mg/day po until symptoms resolveVitamin B3 (Niacin)Chocolate, oats, dates, milk, cottage cheese, eggs, fish, poultry, bananasAbsorbed in intestinesNiacin deficiency can occur where corn is the mainstay of the dietOccurs in industrialized countries in alcoholicsSigns/Symptoms:Anorexia, weakness, irritability , mouth soreness, glossitis, stomatitis, weight lossPellagra Triad: 3 D’s dermatitis, diarrhea, dementiaDiagnosis:N-methynicotinamide in urine can be measuredNAD and NADP can be measured, but are nonspecificTreatment:Niacin or niacinamide 10-150 mg/day poVitamin B6 Deficiency:Meats, grains, nuts, vegetables, bananasMost commonly occurs in patients taking isoniazid, cycloserine, penicillamine, oral contraceptives and in alcoholicsAlso occurs in the elderly, dialysis patients, HIV patients, and patients with rheumatoid arthritis and liver diseaseSymptoms:Seborrheic dermatitis, glossitis, angular cheilitis, confusion, somnolence (similar to other Vitamin B deficiencies)Diagnosis:Plasma pyridoxal phosphate concentration (PLP)Urinary excretion levels of pyridoxic acidTreatment:10-20 mg/day Vitamin B6 Vitamin B9 (Folic Acid)Citrus fruits, grains, legumes, green leafy vegetables and liverDaily requirements are 50-100 mcgPoor diet, alcoholics, overcooking of foodSigns/Symptoms:Megaloblastic and macrocytic anemiasFatigue, HA, palpitationsGray hairMouth ulcersGlossitisDiagnosis:RBC folic acid level<150 ng/mlMacrocytosisHypersegmented neutrophilsElevated LDH and bilirubinNormal B12 levelsTreatment:1mg/day POVitamin B12 Sources: Meat/DairyCauses: strict vegans, alcoholics, elderly, pernicious anemia, H.pylori, metformin, PPI’sSigns/Symptoms:Paresthesias, numbness, tinglingVibration/Position sense lossProprioception/Balance lossDementia, Memory disturbanceFindings:MacrocytosisMegaloblastic anemiaHypersegmented neutrophilsLow serum B12 <170Schilling test (rarely)Treatment:IM or SQ 100mcg daily for first week then weekly for one month followed by monthly for lifeVitamin C (Ascorbic Acid)Fresh fruits and vegetablesPopulations affected: urban/poor, smokers, elderly, alcoholics, chronic illnessSymptoms:Weakness/fatigueScurvy: Perifollicular hemorrhages, petechiae, purpura, hemarthrosis, bleeding gums, splinter hemorrhages, corkscrew hairLate symptoms: Edema, oliguria, neuropathy, intracerebral hemorrhage, deathTreatment:300-1000 mg/dayVitamin A (Retinol)Found in highly pigmented vegetables as beta-carotenes and carotenoidsPopulations: fat malabsorption syndromes, mineral oil laxative abuse, elderly, poorMost common cause of blindness in developing countriesSymptoms:Night blindness, Bitot’s spots and xerosisKeratomalacia, blindness, perforationDiagnosis:Strongly suggestive: night blindnessVitamin A serum levels <30-65Treatment:Orally 30,000 IU QDx7daysVitamin D:Primary food source is fortified milk Populations at risk: infants, elderly, disabled, malabsorption syndromesSymptoms:Nonspecific muscle painRickets in childrenOsteomalacia in adultsLab Findings:25-hydroxyvitamin D (25-OHD) serum level <15-37.5Treatment:600-800 IU vitamin D currently recommended for osteoporosis with 1200-1500 mg calcium per day. Vitamin E:Sources: oils, nuts, avocadoSymptoms:AreflexiaGait disturbancesDecreased proprioceptionDecreased vibratory sensationMyopathyDiagnosis:Plasma vitamin E level <0.5 mg/dLTreatment: 100-400 IU/DayVitamin K:Populations affected: newborn infants, alcoholics, IBD, bulimics, cystic fibrosisSources: green leafy vegetablesMajor Symptom: bleeding from minor traumamucosal and subcutaneous bleeding, epistaxis, hematoma, menorrhagia, GI bleeding, bleeding from gums.Diagnosis:PT/INR elevatedTreatment:FFP Reversal of warfarin effectsHerniasHiatal Hernia:Found in 50% of patients >50Increases in ageSliding hernias more common in women than menAssociated with diverticulosis, esophagitis, duodenal ulcers and gall stonesSymptoms:HeartburnDysphagiaChest PainRegurgitationPostprandial fullnessDyspneaGI bleedWheezingHoarsenessClassified:SlidingParaesophagealMixed (rare)Large- intrabdominal organs enter hernia sacWork-Up:Upper endoscopy to exclude abnormal metaplasia, dysplasia or neoplasiaBarium contrast UGIUpper GI endoscopyTreatment:Lifestyle modifications avoiding caffeine, chocolate, mint, CCB’s, and anticholinergicsWeight lossAvoid large quantities of food with mealsSleep with head of bed elevatedAntacids may be used to relieve mild sxH2 agonists: cimetidine 400mg BID, rantidine 150mg BIDPPI’s: omeprazole 20mg QDProkinetic agents: metoclopramide 10mg taken 30 min before each mealSurgeryLiverViral Hepatitis Symptoms:Prodrome often insidious: malaise, arthralgia, fatigue, anorexia, nausea, vomiting, low-grade feverRUQ/epigastric pain, hepatomegaly, jaundice/icterusVery elevated transaminasesHepatitis A:Transmitted fecal-oral: shellfish, contaminated fruit/vegetables, Incubation period averages 30 daysNo chronic carrier stateDiagnosis:AntiHAV IgM Prevention:Immune globulin availableVaccine:travel to endemic areas (incl. military)food, sewage, daycare/nursing home/veterinary workerspts with underlying chronic liver diseaseMSM, IVDAchildrenHepatitis B:dsDNA genomecore protein (HBcAg)surface protein (HBsAgTransmission: blood, blood products, IVDA, sexualIncubation: 6 weeks to 6 monthsDiagnosis:HBsAg: first evidence of infection (appears before elevated LFTs)anti-HBsAb: appears after clearance of HBsAg or after vaccinationanti-HBcAb: useful when HBsAg cleared but antiHBsAb not yet detectableHBeAg: secretory form of HBsAg. Indicates infectivityPrevention:HBIG if given w/in 7d post-exposure or to newborns of HBsAg + mothersVaccine:HBsAg aloneall medical workers, dialysis, domestic/sexual partners of infected, MSM, IVDA, childrenPrognosis:Acute mortality 0.1-1%, higher with HDV coinfectionChronic in 1-2% of immunocompetent adultsHepatitis D:Only causes hepatitis in co-infection with HBVIn chronic HepB, superinfection with HDV = worse prognosisHepatitis C:Transmission similar to HBV – IVDA is the most common routeIncubation: 6-7 weeks. Often asymptomaticMost frequent indication for liver transplantation8-10k deaths/yearNo reliable means of preventionDiagnosis:anti-HCVAbPCR for HCV RNA - confirmatoryPrognosis: Chronic in 80% Treatment:interferon alpha or peginterferon for 24-48 weeks- depends on viral genotypeRibavirinHepatitis E:RNA virusEnterically transmittedNo carrier stateHigh mortality (10-20%) in pregnant womenConsider if travel Hx.Hepatitis G:Not important cause of liver diseaseChronic viremia lasting >10 yr1.5% of blood donors, 50% of IVDA, 30% of dialysis patientsCirrhosis:Irreversible chronic injury of liver parenchyma with extensive fibrosisTypes:Alcoholic (Laennec’s cirrhosis)PosthepaticCardiac (prolonged, severe, right-sided CHF)Metabolic, Inherited, Drug-relatedPrimary Biliary Cirrhosis (destruction of bile ducts with resulting cholestasis):pruritus, fatigue earlyjaundice and gradual darkening of the exposed areas of the skinsteatorrhea lipid deposition around the eyes (xanthelasmas) and over joints and tendons (xanthomas). Secondary Biliary Cirrhosis (prolonged partial or total obstruction of common bile duct)Complications:Portal hypertensionVariceal BleedingAscitesSpontaneous Bacterial PeritonitisTIPS procedure:Interventional radiology makes a tunnel through the liver with a needle, connecting the portal vein to one of the hepatic veins. A metal stent is placed in this tunnel to keep it open.The shunt allows the blood to flow normally through the liver to the hepatic vein. This reduces portal hypertension, and allows the veins to shrink to normal size, helping to stop variceal bleeding. Child-Pugh Classification of Cirrhosis ** attachmentHepatocellular Carcinoma:Fifth most common cancer worldAreas with high rates of Hep B or C have inc rates Males > femalesPeak incidence: 5th-6th decadeRisk Factors:Chronic liver diseaseCirrhosisChronic B or C infectionHepatotoxins: alcohol, high dose anabolic steroids, possibly estrogenSystemic diseases affecting the liver including hemochromatosis, tyrosinemia and alpha1antitrypsin deficiencySymptoms:1/3 of patients are asymptomaticsigns of underlying cirrhosis present (weight loss, ascites)paraneoplastic syndromes (hypoglycemia, erythocytosis, hypercalcemia, severe diarrhea)Work-Up:LFt’sElevated AFP Ultrasound, CT or MRIPercutaneous biopsy is diagnosticTreatment:Early stage: curative treatment (resection, liver transplant or percutaneous ablation)Intermediate stage: possible chemoembolizationAdvanced stage: no curative treatmentEnd stage: palliative careGall BladderCholelithiasis:Frequently asymptomatic2 Major types: cholesterol (80%) and pigment stoneSymptoms: Biliary Colicpain is characteristically a severe, steady ache or fullness in the epigastrium or RUQ of the abdomen nausea and vomiting frequently accompany episodes of biliary pain. may be precipitated by eating a fatty meal, by consumption of a large meal following a period of prolonged fastingAcute Cholecystitis:inflammation of the gallbladder wall usually follows obstruction of the cystic duct Chronic Cholecystitis:almost always associated with the presence of gallstonesthought to result from repeated bouts of subacute or acute cholecystitis or from persistent mechanical irritation of the gallbladder wall by stonesHydrops - resolution of acute phase but duct obstruction persists. Gallbladder over-distended with clear, mucoid fluidPorcelain gallbladder - d/t calcium depositionSigns/Symptoms:Murphy’s signTriad of RUQ pain, fever, leukocytosisDiagnosis:mildly elevated LFTsRUQ ultrasound: gallbladder wall thickening and pericholecystic fluidHIDA scan: 98% sensitive ................
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