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4/20/2015 ABIM GASTROENTEROLOGY BOARD REVIEW Mark F. Young, M.D. ETSU Quillen College of Medicine I, Mark F. Young, M.D., DO NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of the subject of this presentation. DISCLOSURE STATEMENT OF FINANCIAL INTEREST WHAT DO I NEED TO KNOW? 1 4/20/2015 CASE 1 A 25 year old, white male with a history of Asthma and Allergy Rhinitis presents to the Emergency Department with a food impaction. He has had solid food Dysphagia for two years. He takes over the counter Omeprazole for intermittent GER symptoms. Emergent Endoscopy in the ED reveals the following Endoscopic and Histologic features: 2 4/20/2015 3 4/20/2015 ? A. The condition is curable within 8 weeks. B. This condition is unlikely to occur in patients with atopic predisposition. C. Esophageal Eosinophilia is usually greater than 100 EOS per high power field. D. Summer is the most common seasonal presentation. E. The condition occurs most often in males. WHICH IS TRUE? This condition is unlikely to occur in patients with atopic predisposition. B. Esophageal Eosinophilia is usually greater than 100 EOS per high power field. C. Summer is the most common seasonal presentation. D. The condition occurs most often in males. E. The condition is curable within 8 weeks. 0% 0% 0% 0% Su m m er tio ge al E on di is c Es op ha Th 0% n is un lik el y . os . in op h is ili th a i Th .. . e m e c os on t c di o. tio .. n Th oc e c cu on rs m di tio os .. . n is cu ra bl e ... A. 4 4/20/2015 EOSINOPHILIC ESOPHAGITIS Chronic > allergy / immune mediated 15 Eosinophils per high power field Eosinophilia inhibitor trial persists after proton pump Immunologic triggers food antigen in children and adults EOSINOPHILIC ESOPHAGITIS Atopic Predisposition Male Endoscopic – Concentric mucosal rings / Linear Furrowing / Stricture / White Exudates Most common cause ED – Food Impaction *Dellon E, Gonsalves N, Furuta et al ACG Clinical Guidelines: Evidence based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis Am J Gastroenterol 2013 May; 108 (5): 679-692 CASE 2 A 50 year old, white male presents for intermittent dysphagia to solids. He has no reflux symptoms. He has no weight loss or blood in the stool. Esophagram is performed. 5 4/20/2015 THERAPY FOR THE ABOVE PROBLEM WOULD INCLUDE ALL OF THE FOLLOWING, EXCEPT: Su rg ic a l c r r e c. . . 0% tio n fo ... re s su pp ila wi th cid f a ge al d ila t io n tia t io n o In i Es op ha 0% d Repeated dilation for recurrent symptoms 0% n of h e. .. D. 0% ct io Surgical correction of hernia or re C. at ed Initiation of acid suppression after dilation pe B. Re Esophageal dilation with large diameter dilator (50 French) .. . A. LOWER ESOPHAGEAL RING: Intermittent Recurrent dysphagia to solids. therapy may be needed Some studies indicate PPI’s may delay reformation of ring “Steak House Syndrome” *Sleisenger, Feldman et al 2010 6 4/20/2015 Long-term acid suppressive therapy may prevent the relapse of lower esophageal (Schatzki's) rings: a prospective, randomized, placebo-controlled study. *Sgouros SN, Vlachogiannakos J, Karamanolis G, Vassiliadis K, Stefanidis G, Bergele C, Papadopoulou E, Avgerinos A, Mantides A, . - Am. J. Gastroenterol. - September 1, 2005; 100 (9); 1929-34 CASE 3 An 80 year old male complains of a two year history of regurgitation of undigested food. His wife states halitosis is a significant problem. He states he maintains good oral hygiene. When swallowing liquids, there is gurgling in the back of throat. No anorexia, no weight loss, no tobacco or alcohol use. WHAT IS THE ETIOLOGY OF THE PROBLEM? Esophageal Cancer C. Longstanding Reflux D. Gastric Inlet Pouch E. Restrictive Myopathy of the Cricopharyngeus Muscle 0% 0% 0% 0% 0% cc id en t ge al C an ce sta r nd in g R Ga ef st Re lu r x st ic ric In le t iv t P e ou M yo ch pa th y o f . .. Cerebral Vascular Accident B. Ce re b Lo ng Es op ha ra l V as cu la r A A. 7 4/20/2015 HYPO PHARYNGEAL DIVERTICULUM (ZENKERS) Most common manifestation of Cricopharyngeal Dysfunction Elderly Area weakness posterior midline region pharyngoesophageal wall Triangle of Killian Definitive treatment – Cricopharyngeal Myotamy *Cook and Kahrilas 1999 TRIANGLE OF KILLIAN ZENKERS 8 4/20/2015 CASE 4 A healthy 60 year old man presents for dysphagia to solids and liquids of a three year duration. He has regurgitation of food and fluid at night and halitosis. He has non-exertional chest pain and weight loss. Esophagram is performed. THE NEXT APPROPRIATE DIAGNOSIS STUDY WOULD BE: er E Up p 0% al 0% er r PI 0% Re f st C he ty o f Sc an l M ot ili CT ge a Es op ha 0% St ud y 0% EN T ENT Referral sc op y Empiric Trial BID PPI E. l B ID P D. nd o Upper Endoscopy ria Esophageal Motility Study C. c T CT Scan of Chest B. Em pi ri A. 9 4/20/2015 THE BEST THERAPEUTIC OPTION FOR THIS PATIENT IS: A. Calcium Channel Blocker B. Endoscopic Injection Botulinum C. Laparoscopic Myotomy D. Esophageal Dilation over Guidewire with Bougie E. Large Diameter “BAG” Dilatation er 0% 0% pa r je ct io lo ck 0% La ha nn el B c I n C c iu m sc op i Ca l En do 0% n Bo os t.. co Es . pi op c M ha yo ge to al m D La y i la rg tio e Di n ov am e. et . . er “B AG ” D i.. . 0% ACHALASIA MONOMETRIC TRIAD: Poorly relaxing LES to swallow Hypertensive LES Lack of peristalsis in esophagus in response to swallowing ACHALASIA: Always rule out secondary achalasia – Esophageal Malignancy with Endoscopy Chagas Disease South America Myotomy better for young patients Botulinum Temporizing *Francis DL, Katzka DA, Achalasia; update on the disease and it’s treatment; Gastroenterology 2010; 139 (2): 369-379 10 4/20/2015 TISSUE TAKEN FROM THIS PATIENT’S LOWER ESOPHAGEAL SPHINCTER WOULD REVEAL A LACK OF WHICH NEUROTRANSMITTER? 0% e e 0% lin na dr e e ch ol in nc e 0% yl Su bs ta 0% Ac et P 0% No ra Noradrenaline n Nitric Oxide E. xid Motilin D. tri c O Acetylcholine C. Ni Substance P B. M ot ili A. ACHALASIA: Cause of primary achalasia unknown Postganglionic Tissue Also denervation of smooth muscle from these patients lack nitric oxide decrease inhibitory neurotransmitter VIP CASE 5 A 16 year old, white female presents for acute onset of painful swallowing over 24 hours duration. She recently saw her dermatologist and was prescribed Doxycycline for acne. She is a diabetic. Upper Endoscopy and esophagram are performed. 11 4/20/2015 THE NEXT MOST APPROPRIATE STEP WOULD BE: A. Nystatin swish and swallow B. Swallowed Fluticasone C. Discontinue Doxycycline D. High dose oral PPI E. Repeat Upper Endoscopy in 8 weeks 0% 0% 0% Di sc ish a w sw in Sw all o Ny st at 0% nd sw al lo w ed Fl ut on ic a t in so ue ne D ox yc yc Hi lin gh Re e do pe se at o U ra pp l P er PI E nd os co py in 0% PILL ESOPHAGITIS: Mid-Esophageal Tetracycline, Quinidine DC erosions Iron, Bisphosphonates, NSAI, K+, offending agent Topical relief “GI Cocktail” 12 4/20/2015 Esophageal Disorders Caused by Medications, Trauma, and Infection *Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Chapter 46, 763-772.e5 CASE 6: 47y M seen in the ER w/ 1 week of odynophagia associated with abdominal pain, n/v, diarrhea and low-grade fever. He has lost 10lbs during this time. Medications include prednisone, tacrolimus, and mycophenolate mofetil taken for a kidney transplant he received 6 months ago. He has no HIV risk factors or other medical problems. PE: 148/94 mmhg, 90/min, 100.8 F EGD: 2.5 cm esophageal ulcer with raised borders, biopsy shows inflammatory infiltrates with granulation tissue associated with inclusion body cells, the remainder esophagus appears normal WHAT IS THE LIKELY DIAGNOSIS? git i s 0% so ph a ag i tis 0% ed E s al ov i git i so ph a a e om eg Cy t di d Ca n 0% ru s 0% nd uc Pill-induced Esophagitis l‐i HIV esophagitis D. P il Cytomegalovirus C. so ph Candida esophagitis B. HI V e A. 13 4/20/2015 INFECTIOUS ESOPHAGITIS Common in Immunsuppressed Pts. (HIV/AIDS, chemo, systemic steroids, etc.) Immunocompetent Most (Inhaled Corticosteroids) Common Pathogens Candida (2/3 will also have oral thrush) HSV/CMV (less likely to have oral lesions) INFECTIOUS ESOPHAGITIS See thrush? Treat w/ fluconazole No Thrush? EGD w/ brushing, biopsy, etc. to establish definitive diagnosis NO Barium Swallow (Nonspecific) HSV ESOPHAGITIS 14 4/20/2015 CANDIDA ESOPHAGITIS CMV INCLUSION BODY CASE 7 A 45 year old, white male is evaluated for chest pain which proves to be non cardiac. His internist institutes a trial of Omeprazole 40mg twice a day which was of no help. Upper Endoscopy reveals a small hiatal hernia. Esophageal Manometry reveals Nutcracker Esophagus. 15 4/20/2015 WHAT IS THE BEST APPROACH FOR SYMPTOM RESOLUTION? Nitrates B. Calcium Channel Blocker C. Benzodiazepine D. Continue PPI another twelve weeks E. Serotonin-Norepinephrine Reuptake Inhibitor 0% 0% 0% 0% 0% Ca l c iu m C Ni tra te ha s nn el B lo c ke Be Co r n nt zo in di ue az ep P PI in Se a e no ro to th ni e r n‐ t. No .. re pi ne ph r i. . A. NON CARDIAC CHEST PAIN Visceral Hypersensitivity Omeprazole test essentially rules out Esophagus as a cause Most have nonspecific findings on motility (except Achalasia) NON CARDIAC CHEST PAIN Treatment: Longer Little therapy with PPI provide no benefit data to support Nitrates Calcium Channel Blockers only temporary Pain modulators best option-SNRI, Tricyclics, Trazodone, SSRI’s *Herghcovice T, et al Aliment Pharmocol Ther 2012; 35: 5-14 16 4/20/2015 CASE 8 A 50 year old, white male with centripetal obesity and GER for 15 years presents for evaluation. He wants to be screened for Barretts. He has no Dysphagia. Upper Endoscopy reveals the following: SHOULD UPPER ENDOSCOPY HAVE BEEN PERFORMED? No 0% 0% No Yes B. Ye s A. 17 4/20/2015 HIS ANNUAL RISK OF ADENOCARCINOMA IS: 20% C. 2% D. .5% 0% 0% 20 % 5% 0% 0% .5 % 5% B. 2% A. HIGH GRADE DYSPLASIA IS REPORTED BY THE PATHOLOGIST. THE NEXT STEP IS: Repeat Endoscopy in one year C. Confirmation by expert pathologist D. Repeat Endoscopy in six months E. Radio Frequency Ablation 0% 0% 0% 0% 0% ge nd ct os om co y py in on at io e .. . n Re by pe ex at E pe nd rt .. os . co Ra py di in o Fr si eq x. .. ue nc y A bl at io n Esophagectomy B. fi r m Co n Re pe at E Es op ha A. 18 4/20/2015 BARRETTS ESOPHAGUS Columnar Male ? Epithelium in the Tubular Esophagus / White / Centripetal Obesity / Chronic GER Endoscopy in correct population BARRETTS ESOPHAGUS 30 – 50 Fold increased risk of Adenocarcinoma Annual incident of .5% Overall survival comparable to age and gender matched population Repeat Endoscopy in one year thin there to five years Low Grade Dysplasia – Confirmed – 6-12 months High Grade Dysplasia – Confirmed – EMR/RFA/Surgery *The Role of Endoscopy in Barretts Esophagus. Volume 7G, No. 6: 2012 Gastrointestinal Endoscopy CASE 9 A 50 year old, white male presents for epigastric pain of three weeks duration. The pain is relieved by antacids. He takes Goody Powders for headache. There is no blood in stool or weight loss. 19 4/20/2015 THE MOST APPROPRIATE WORKUP COULD INCLUDE THE FOLLOWING EXCEPT: St oo l A 0% sio ico b. .. n 0% pp re s te r er E ba c 0% Su 0% Up p ico H el or og y f ro l Se Di sc o nt in ui ng Go od y P o. .. 0% Ac id Start Acid Suppression St ar t Stool Antigen for Helicobacter E. sc op y Upper Endoscopy D. fo r H el Serology for Helicobacter C. nd o Discontinuing Goody Powder B. nt ige n A. CASE 10 Stool antigen for Helicobacter is positive. The patient was treated for a sinusitis several months ago with a macrolide antibiotic. YOU SHOULD TREAT THIS PATIENT WITH: BID PPI/Clarithromycin/Amoxicillin B. BID PPI/Clarithromycin/Flagyl C. BID PPI/Bisthmyth/Metronidazole/ Tetracycline D. Levofloxacin/Amoxicillin/PPI E. Bismuth/PCN 0% 0% 0% 0% 0% BI D PP I/C la r it BI hr D om PP I/C yc in la r it ... BI h ro D PP m yc I/B in ist /F Le hm . .. vo yt flo h/ xa M c in et r. . /A . m ox ici lli n. .. Bi sm ut h/ PC N A. 20 4/20/2015 THE FOLLOWING ARE TRUE STATEMENTS ABOUT HP EXCEPT: ra .. . he st om ac h. .. n t on E uo ... 0% p i on c m m 0% ee of d to ch i n ns hi p d i ire A co at io el Ac qu e r In ve rs 0% d Lives deep in the stomach lining 0% se E. 0% w or e GER may be wore on Eradication au D. ay b e A common cause of duodenal ulcer L iv es Acquired in childhood C. GE R m B. so . .. Inverse relationship to socioeconomic status ld ho od A. DYSPEPSIA: Discomfort nausea in mid abdomen with bloating and Functional-No relief with Acid suppression PUD/GER/Malignancy/Biliary Tract Disease WARNING SIGNS: Dysphagia Odynophagia Fe Deficiency Anemia Jaundice GI Bleed Lymphadenopathy Family history Cancer Proximal Tract 21 4/20/2015 WORK UP: NSAI or GER – Stop Agent and TX PPI < 55 No Alarms – Test and Treat – HP > 55 or Alarm - EGD HELICOBACTER Gram Strong Risk negative Microaerophilic Rod Urease producer factor for Gastric Malignancy Old Age/Inverse relationship Socioeconomic status TREATMENT AND TESTING You should be aware of Macrolide Resistance!!! You should be aware of limitations of testing!!! 22 4/20/2015 WHEN DO WE DOCUMENT ERADICATION? Complicated Personal Need PUD (Bleeding or Perforation) history of Gastric Cancer for future NSAID REFERENCES Chey WD, Wong BC; Practice parameters committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter Pylori Infection; AM J Gastroenterol 2007; 102: 1808-1825 Luther J, Higgins PD, Schoenfeld PS, Moayyedi, Vakil N, Chey WD, Empiric Quadruple vs Triple Therapy for primary treatment of Helicobacter Pylori Infection; AM J Gastroenterol. 2010 Jan 105 (1): 65-73 CASE 11 A 30 year old, white female presents for Chronic Diarrhea. She is rather thin and states intentional weight loss has been an issue and is using osmotic laxatives. Stool leukocytes are negative. 23 4/20/2015 WHICH OF THE FOLLOWING VALUES WOULD BE MOST CONSISTENT? Fecal Na 50mmol/L, K+mmol/L, Stool 290 Osmol B. Fecal Na 50mmol/L, K+ 30mmol/L, Stool 230 Osmol C. Fecal Na 100mmol/L, K+ 30mmol/L, Stool 290 Osmol D. Fecal Na 150mmol/L, K+ 75mmol/L, Stool 480 Osmol E. Fecal Na 45mmol/L, K+ 60mmol/L, Stool 290 Osmol 0% 0% 0% 50 m al N a l N a 0% Fe c Fe ca 0% m ol /L , K +m 50 . .. m Fe m ol ca /L l N , a K+ 10 .. 0m . Fe ca m ol l N /L a , K 15 +. 0m Fe .. ca m l N ol /L a , K 45 +. m .. m ol /L , K + . .. A. OSMOTIC DIARRHEA Calculate Normal Gap Gut Osmolality – 2 (Fecal Na + Fecal K+) (290mosm/kg) > 50 mosm/kg is Osmotic Diarrhea Osmotic Laxatives / Carbohydrate Malabsorption SECRETORY DIARRHEA Small Osmotic Gap Stool Osmolality Physiologically 290 mosm/kg *Contaminated Stool with water/Osmolaliy <290 *Contaminated with urine Stool Osmolality >290 High Volume Persists with fasting *Sleisenger and Fordtran Gastrointestinal and Liver Disease 2010 p211-232 24 4/20/2015 CASE 12 A 22 year old, white female presents for 16 months of watery diarrhea and bloating. Bloating improves after bowel movement. No travel. No family history of GI Disease. No weight loss, anemia, melena, or floating stools. Physical exam is normal. Her friend was recently diagnosed with Celiac Disease and she is concerned. WHAT IS THE BEST INITIAL TEST TO EVALUATE FOR CELIAC? C. D-xylose Absorption Test D. IgA Tissue Transglutaminase Antibody E. HLA Genotyping 0% 0% 0% 0% 0% G lia di n An t ib m id od at ie ed s D‐ G xy lu lo te se n . Ab Ig .. A T so rp iss t io ue n T T ra es ns t gl ut am in HL a. . A G en ot yp in g IgG Deamidated Gluten Peptides Ig A IgA Gliadin Antibodies B. Ig G De a A. IS UPPER ENDOSCOPY TRULY NECESSARY TO CONFIRM A DIAGNOSIS OF CELIAC DISEASE? No 0% 0% No Yes B. Ye s A. 25 4/20/2015 She goes on a Gluten Free Diet after Consultation with the Dietician. She does extremely well until two years later when diarrhea begins again. THE MOST LIKELY CAUSE OF HER SYMPTOMS IS: De v ge s.. . S in pr u ge n te n g I B 0% e 0% ou s S Co ... ic 0% la icr M ia te d 0% As so c el op m en t o f L os co p ym ph om a 0% nt G lu Inadvertent Gluten ingestion dv er te Collagenous Sprue E. In a Overriding IBS D. r id in Associated Microscopic Colitis C. Ov er Development of Lymphoma B. Co l A. CELIAC DISEASE Small intestine malabsorption of nutrients after ingestion of wheat, gluten or related proteins from rye or barley HLA-DQ2 or HLA-DQ8 Haplotype Remember diarrhea and iron deficiency!!! 26 4/20/2015 CELIAC ASSOCIATION Autoimmune Type Thyroid Disease 1 Diabetes – 10% Unexplained Premature Increase Transaminase Elevation Osteoporosis Lymphoma Risk CELIAC DIAGNOSIS IgA test Tissue Transglutaminase Antibody preferred >95% sensitivity and specificity Small Bowel biopsy necessary to confirm *IgA Gliadin Antibodies No Role* If low IgA Level, use IgG Testing or HLA Genotyping CELIAC Noncompliance with diet most likely cause of refractory symptoms D-Xylose low – Mucosal Disease D-Xylose normal – Suspect Pancreatic Disease Be on the look out for Dermatitis Herpetiformis *Rubio-Tapia A, Hill IO, Kelly CP et al ACG Guidelines: Diagnosis and Management of Celiac Disease AM J Gastroenterol 2013; 108 (5) 656-676 27 4/20/2015 DERMATITIS HERPETIFORMIS CASE 13 A 40 year old, white male had twenty centimeters of small intestine resected after a motor vehicle accident. He now has diarrhea. 28 4/20/2015 THE MOST LIKELY CAUSE IS: Crohns Disease C. Bile Salt Malabsorption D. Steatorrhea E. IBS 0% 0% 0% 0% Cr o Ce li 0% IB S Celiac Disease B. ac D ise as e hn Bi s D le Sa ise lt as M e al ab so rp tio n St ea to rr he a A. ILEAL RESECTION < 100cm TI – Loss of Bile Salt Absorption – Hepatic Overproduction – Questran >100cm TI Resection – Bile Salt DeficiencySteatorrhea CASE 14 A 29 year old, white male presents with bloody diarrhea of two weeks duration. He has had associated Arthralgia with weight loss. He also has experienced Pneumaturia. Physical exam reveals no abnormalities except mild guarding in the right lower quadrant. Labs reveal iron deficiency anemia. Stool studies are negative. He is FIT positive and ASCA positive and ANCA negative. Barium x-ray is performed. 29 4/20/2015 COLONOSCOPY AND BIOPSY WOULD LIKELY REVEAL? D. Arteriovenous Malformation E. Mucosal Disease Only 0% 0% 0% 0% ul o Co l e er t ic n th In vo l Di v as ” i M or e re A kip “S 0% sis en r io t i n ve “W no ... us M alf M or uc m os a. al .. D ise as e On ly More Involvement in “Watershed” areas Ar te Diverticulosis C. on “Skip Areas” in the Colon B. ve m A. COLONOSCOPY IS PERFORMED AND REVEALS CROHNS DISEASE WITH A FISTULA TO THE URINARY BLADDER. TREATMENT WOULD CONSIST OF: Infliximab B. Mesalamine C. Cyclosporine D. Steroid Enemas E. Masalamine Suppositories 0% 0% 0% 0% 0% In fli xim ab M es al am in e Cy c lo sp or in St e M er as oid al En am em in e S as up po sit or ie s A. 30 4/20/2015 CROHNS DISEASE Trans Skip mural Inflammation Lesions *Stricture/Fistula/Abscess ASCA Positive 50 % Crohns Patients Increase CRP CROHNS DISEASE - TREATMENT Fistula – Infliximab/Adalimumab/Certolizumab Small Bowel Disease – MTX/6MP/Azathioprine/Biologics/Budesonide/Steroids Colon - Mesalamine ULCERATIVE COLITIS Bloody Diarrhea/Tenesmus Weight Loss pANCA Positive 77% Mucosal/Disease Limited to Colon 31 4/20/2015 ULCERATIVE COLITIS- TREATMENT Mesalomine – First Line Prednisone/Immune Colectomy Modulators/Biologics Curative!!! IBD - KNOW THE FOLLOWING Begin screening after 10 years Colonic involvement Confirmed low grade Dysplasia equals Colectomy Antiperistaltics in U.C. can precipitate Toxic Mega Colon which equals surgery Surgery Crohns is curative in Ulcerative Colitis and avoided in AZOTHIOPRINE / 6MP Pancreatitis Leukopenia Hepatosplenic Latent T Cell Lymphoma TB (Screen Prior to Starting) Reactivation of Hepatitis B 32 4/20/2015 IBD – KNOW THE FOLLOWING Improvement with Disease Control: Do Not Improve with Disease Control: • Pyoderma Gangrenosum • Sacroileitis • Erythema Nodosum • PSC – Increased AP • Peripheral Arthritis • Ankylosing Spondylitis • Uveitis *Urogenital Complications of Crohns Disease. AM J Gastroenterol 2006; 101: S640-S643 *Sandborn WJ Infliximab for induction and maintenance therapy for Ulcerative Colitis N Engl J Med 2005; 353: 2462-76 PYODERMA GANGRENOSUM 33 4/20/2015 ERYTHEMA NODOSUM UVEITIS CASE 15 A 50 year old, white male presents for Colon Cancer Screening. He would like to know options offered by the U.S. Preventative Task Force. 34 4/20/2015 THEY INCLUDE ALL OF THE FOLLOWING EXCEPT: D. Stool Guaiac Testing 0% 0% . .. gm oid nn ua l T A ve ry 1 0 ye 0% Fle xi bl e Si py e St oo l F I on os co Co l 0% es t in g Flexible Sigmoidoscopy every 5 years ... C. T Colonoscopy every 10 years and continue until age 75 St oo l G ua iac B. os co py e Stool FIT Annually ly A. COLONOSCOPY IS PERFORMED AND REVEALS TWO TUBULAR ADENOMAS (<1CM) REPEAT COLONOSCOPY SHOULD BE PERFORMED IN: 6 Months 1 Ye a r 0% 0% 0% 0% hs 10 Years D. 6 M on t 5 Years C. rs B. 10 Y ea 1 Year 5 Ye ar s A. POLYP FOLLOW UP RECOMMENDATIONS: < 3 Tubular Adenomas < than 1cm No FH Colon 5 Years Multiple Adenomas/Large Adenoma > 1cm/Villous Histology/High Grade Dysplasia or Positive Family History Repeat 3 Years *Hyperplastic* routine CRC 10 Years SSA – Increased risk of missed Right Colon Cancers *U.S. Multi-Society Task Force on Colorectal Cancer 35 4/20/2015 STOOL FIT Detects human globin More specific for human blood No false negative with vitamin C Preferred cancer detection test No randomized trial where outcome is CRC Questionable better adherence *Morekowa T, Kato S, Yamaji, Et al A Comparison of Immunochemical Fecal Occult Blood Test and Total Colonoscopy in Asymptomatic Population Gastroenterology 2005; 129 422-4285 SCREENING/SURVEILLANCE RECOMMENDATIONS FOR FAP PATIENTS APC gene mutation + At-risk individuals Annual FS starting at age 12 APC gene mutation Genotype not available FS at age 25 Age 12: annual FS Age 25: FS every 2 years Age 35: FS every 3 years Age 50: follow screening for average-risk patients Retained rectum: FS every 6 months Affected individuals Retained J-pouch: FS every 1-2 years Annual physical exam and routine blood tests Upper GI surveillance every 3-4 years; annually if polyps found Adapted from Cruz-Correa M, et al. Gastroenterol Clin N Am. 2002;31:537. EXTRACOLONIC FEATURES OF FAP AND HNPCC Other lesions Extracolonic Cancers in FAP Duodenal (5%-11%) Pancreatic (2%) Thyroid (2%) Brain (medulloblastoma) < 1% Hepatoblastoma (0.7% of children years old) Extracolonic Cancers in HNPCC <5 Congenital hypertrophy of the retinal pigment epithelium (CHRPE) Nasopharyngeal angiofibroma Osteomas Radiopaque jaw lesions Supernumerary teeth Lipomas, fibromas, epidermoid cysts Desmoid tumors Endometrial (39-60% Stomach (12-19%) Gastric adenomas/fundic gland polyps Ovarian (9%) Duodenal, jejunal, ileal adenomas Ureter and renal pelvis (4-10%) Café au lait spots Biliary tract (2-18%) Sebaceous gland adenomas, carcinomas Brain (glioblastoma) (4%) Keratoacanthomas Small bowel (1-4%) Endometrial (39-60%) Adapted from Cruz-Correa M, et al. Gastroenterol Clin N Am. 2002;31:537. 36 4/20/2015 CASE 16 A 42 year old, female is admitted with epigastric pain, nausea and emesis. On exam, she is Afebrile with a heart rate of 150 beats per minute. Her abdomen is diffusely tender. WBC count is 15,000 with a left shift. HCT 47, BUN 28mg/dl, Serum Cr 1.0 with normal Liver Function Tests. Amylase 5200, Lipase 2800. A diagnosis of Acute Pancreatitis is made. ALL OF THE FOLLOWING PREDICTS SEVERITY EXCEPT: A. Ranson’s Scoring System takes 48 hours to complete B. Marked elevation of Amylase and Lipase predict severity C. Apache-0 is useful in severity assessment D. SIRS identifies patient with increased mortality E. Initial and subsequent BUN levels can predict severity 0% 0% 0% 0% co r el e ke d Ap ac M ar Ra ns on ’s S va t in g S ys te m ... io n o he f A ‐0 is m y us ... SI ef RS ul id in en se t if ve ie In . .. s p iti at al ie a nt nd w su i .. bs eq ue nt B .. 0% PANCREATITIS Ranson/Glasgow Apache take 48 hours to complete II accurate at 24 hours Apache-0 added BMI Admission BUN >25mg/dl and BUN increase of 5mg/dl in first 24 hours – Increased Mortality!!! Amylase and Lipase levels do not predict severity *WUBU et al Early changes in blood urea nitrogen predict mortality in Acute Pancreatitis Gastroenterology 2009; 137: 129-36 37 4/20/2015 CASE 17 A 65 year old man is admitted with severe abdominal pain, fever, nausea and vomiting. On examination he is febrile, with stable vital signs. The upper abdomen is diffusely tender, with rebound and absent bowel sounds. Left flank ecchymosis is present. Serum amylase and lipase are elevated. After aggressive fluid resuscitation, a contrast CT scan on day 2 of illness demonstrates an edematous pancreas with non enhancement of about 30% of the gland and multiple peri-pancreatic fluid collections. IN TERMS OF MANAGEMENT, WHICH OF THE FOLLOWING STATEMENTS ABOUT NUTRITION IS CORRECT? p ar ta l . sis co nt r.. n. .. p. .. e 0% ec ro t io ut ri 0% n is th t io is ut ri or t l n ra up p l s To en te t io na ta l p ar To Nu tri 0% re at ic n Pancreatic necrosis contraindicates enteral feeding 0% l n E. 0% ra Enteral nutrition is the preferred route for nutritional support in patients with severe acute pancreatitis iti o D. l n ut r Total parenteral nutrition is associated with mortality reduction in acute pancreatitis En te ra C. Pa nc Nutritional support is indicated in patients with mild pancreatitis to reduce complications ... B. in d. .. Total parenteral nutrition and enteral nutrition result in similar metabolic complications en te A. PANCREATITIS/FEEDING Mild Pancreatitis - Hydration Alone Initial Feeding with low fat diet is Safe Enteral Feeding is Safe and Tolerated in Acute Pancreatitis Enteral Feeding may preserve barrier function Improved outcomes with Enteral Feeding compared to Parenteral Feeding with less infectious complications reduce cost and better Glycemic control *Petrov MS, van Santvoort HC, Besselink MS, et al Enteral nutrition and the risk of mortality and infectious complications in patients with severe acute pancreatitis: a meta-analysis of randomized trials. Arch Surg 2008; 143: 1111-17 38 4/20/2015 CASE 18 A 80 year old male is admitted with sever epigastric pain, radiating to the back with nausea and vomiting. He is febrile with a blood pressure of 120/80 an a pulse of 110. WBC 20,000, AST 300, ALT 400, ALK FOS 245 and Total BILI 5, Lipase 5,000. Ultrasound reveals multiple gallstones in the Gallbladder and a Common Bile Duct size of 14mm. Antibiotics and IV fluids have begun. WHAT IS THE NEXT STEP? Serial Amylase and Lipase Levels E. Emergent ERCP 0% on su l f A bd om y C o Sc an Su rg er CT 0% 0% 0% 0% En l.. . te ra ria l N l A ut m rit yl as io n e an d L ip as . Em .. er ge nt E RC P Enteral Nutrition D. Se C. nd . .. Surgery Consult for Cholecystectomy r C ho B. en a CT Scan of Abdomen and Pelvis t f o A. GALLSTONE PANCREATITIS Early Biliary Sphincterotomy is beneficial in SEVERE Acute Biliary Pancreatitis Early ERCP not beneficial with mild Biliary Pancreatitis and absence of Biliary Obstruction With clinical deterioration, suggestive of Ascending Cholangitis – ERCP recommended *Petrov MS, van Santvoor HC, Besselink MG, et al. Early endoscopic retrograde cholangiopancreatography versus conservative management in acute biliary pancreatitis? A meta-analysis of randomized trials. Ann Surg 2008;247:250-57 39 4/20/2015 CASE 19 A 65 year old male with a mechanical aortic valve repair for aortic stenosis presents to the emergency room with painless hematochezia. He is on Coumadin, and takes Aspirin 81mg daily. He is volume resuscitated with at least 6 units of packed RBCs, and stabilized. An urgent Colonoscopy is performed which demonstrates no fresh blood in the terminal Ileum or Colon. There are a few small, scattered diverticuli. WHAT WOULD YOU DO NEXT? nd o 0% 0% 0% y Sc an 0% d R BC er E Up p Ta gg e sc op y 0% Su rg er Surgery g Angiography E. ap hy Nothing D. og r Tagged RBC Scan C. An gi Upper Endoscopy B. No th in A. GI BLEEDING Up to 18% of cases of significant Hematochezia are presentations of Upper GI Bleeding. “Silent Ulcer” – Aspirin, greater than age 60 40 4/20/2015 HEMATOCHEZIA ? EGD FIRST ? Significant High Hemodynamic Compromise Volume Requirements for Resuscitation Large Magnitude of Decrement in Hematocrit Clinical Risk Factors for Peptic Ulceration or Portal Hypertension *Rockall TA, Logan RF, Devlin HB, et al. Risk management after acute upper gastrointestinal hemorrhage. Gut 1996; 38:316-21 TOXICITY OF PROTON PUMP INHIBITORS Hip Fracture – Retrospective Study Hypomagnesaemia Increased Serum Gastrin Levels Increased Risk of C-Diff Infection if Hospitalized Short Term Use – Pneumonia CASE 20 A 60 year old female presents for evaluation of increasing abdominal girth. She states that she has two glasses of wine per week. She is not overweight. She states that she had “yellow jaundice” as a child. Ultrasound of her abdomen reveals significant Ascites. Echo reveals an ejection fraction of 75%. Paracentesis is performed. Serum Albumin is 4.0gr/dL. Ascitic Albumin is 3.1gr/dL. No evidence of SBP. The fluid is sent for Cytology. 41 4/20/2015 HER MOST LIKELY DIAGNOSIS IS: 0% 0% e H Ov ea ar ia rt n F a Ca ilu nc re er w ith M ... ec 0% ar y C irr ... Pr im ar ho sis S Ci rr 0% ho s is 0% tiv Ovarian Cancer with METS Omentum y B ili Congestive Heart Failure E. ge s Primary Biliary Cirrhosis D. Co n C. NA FL D Cirrhosis Secondary to Alcoholism y t o A NAFLD B. on da r A. KNOW THE SERUM – ALBUMIN GRADIENT Serum Albumin – Ascitic Albumin 1.1gm/dl or Greater – Portal Hypertension or CHF Total Ascites Protein Greater than 2.5gm/dl Heart Failure or Constrictive Pericarditis SAAG Less than 1.1gm/dl – Malignancy, Infection *Runyon, BA; AASLD Practice Guidelines Committee. Management of adult patients with Ascites due to Cirrhosis: an update. Hepatology, 2009; 49(6): 2087-2107. CASE 21 A 50 year old male with diabetes presents with elevated liver enzymes. His physical activity level has recently decreased due to increasing pain in joints including arthritis in his hands. AST 84 IU/L, ALT 60 IU/L, ALP 120 IU/L, T bili 0.9 mg/dl. ANA 1:20, smooth muscle ab neg, IgG quant 1503. HBsAg neg, HBsAb positive, HCV ab negative, Iron is 143 ug/dL, Transferrin saturation 62%, Ferritin 803 ug/L. A liver biopsy is performed. 42 4/20/2015 WHICH OF THE FOLLOWING COMPLICATIONS OF THIS DISORDER IS MOST LIKELY REVERSIBLE WITH TREATMENT? Cirrhosis E. Risk of HHC in the setting of Cirrhosis 0% 0% 0% 0% 0% Ci rr ho sis se tti ng . . Cardiac Dysfunction D. t h e Hypogonadism C. Ri sk of H HC in Arthropathy B. Ar th ro pa th Hy y po go Ca na rd di sm iac D ys fu nc tio n A. HEMOCHROMATOSIS Diagnosis Transferrin saturation > 50% Liver biopsy to assess hepatic iron level (Hepatic iron index) Genetic testing for HFE Treatment Phlebotomy to reduce iron content of the body If iron stores normalize before fibrosis of liver then normal life expectancy Once cirrhosis develops then high risk of hepatoma SCREEN ALL FIRST DEGRE RELATIVES!!! 43 4/20/2015 HEMOCHROMATOSIS-COMPLICATIONS Reversable: Nonreversible: • Cardiac Dysfunction • Cirrhosis • Glucose Intolerance • Risk of HCC after Cirrhosis • Hepatomegaly • Arthropathy • Skin Pigmentation • Hypogonadism • Early Fibrosis *Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology. 2011;54(1):328 CASE 22 You are asked to see a 65 year old man admitted 36 hours prior due to worsening Dyspnea, Palpitations and feeling faint. On admission, his HR is 165 and blood pressure is 70/40. The patient has a known history of ASCVD with prior right ventricular infarction 6 months ago, and atrial fibrillation for which he was recently started on amiodarone. You are consulted for evaluation of elevated liver tests: ALT 4,600 U/L, AST 6,900 U/L, Alkaline Phosphatase 180 U/L, Total Bilirubin 0.9 mg/dL, Albumin 3.2 g/dL, INR 2.3. The patient’s history is also positive for Diabetes and Dyslipidemia. Echocardiogram done on admission shows PAP 79/43, dilated RV, and dilated LV with EF of 35%. THE MOST LIKELY CAUSE OF THE ABNORMAL LFT’S IS: Acute Viral Hepatitis E. Acute Biliary Obstruction 0% 0% 0% 0% 0% ba l U se m ic H ep at e H it i ep s at ot Ac ox ut ici e V ty Ac ira ut l H e B ep ili at ar iti y O s bs tr uc t io n D. ro n Amiodarone Hepatotoxicity us H er Ischemic Hepatitis C. Isc he B. Am io da Surreptitious Herbal Use ep t it io A. Su rr 44 4/20/2015 ISCHEMIC HEPATITIS Clinical picture for right heart failure Hepatocellular enzymes in the thousands Can also be seen in ICU post code Also consider in patients found unresponsive outside the hospital *Taylor RM, Tujios S, Jinjuvadia K, et al. Short and long-term outcomes in patients with acute liver failure due to ischemic hepatitis. Dig Dis Sci 2012;57(3):777-85 CASE 23 A 26 year old woman presents with altered mental status and jaundice. Her parents state that she has no history of depression, but has had trouble with academics and difficulty concentrating in school. Her parents believe she may have ADHD. Oral contraceptives are her only medication and she has not taken any new medications recently. Alk Phos 72 IU/L, T Bili 15.1 mg/dL, D bili 6.0 mg/dL, INR 2.3, AST 605 IU/L, ALT 351 IU/L, Hgb 9 g/dL, ceruloplasmin 24, IgG 1703. Color Doppler US of liver is normal. WHICH LABORATORY STUDY IS MOST LIKELY TO CONFIRM THE DIAGNOSIS? Serum Acetaminophen Level D. Anti-nuclear Antibody E. Hypercoagulable Workup 0% 0% 0% 0% 0% U rin ar y Co ru pp m er A ru lc o m A ho ce l L ta ev m el in op An he t i‐ n nu L.. . c l Hy ea r A pe rc nt oa ib od gu la y bl e W or ku p Serum Alcohol Level C. Se B. 24 hr 24hr Urinary Copper Se A. 45 4/20/2015 WILSON’S DISEASE Decreased serum ceruloplasmin level Increased urinary copper level Excessive hepatic copper level KAYSER FLEISCHER RING (copper deposit in cornea) Treatment D-penicillamine or trientine Fulminant hepatitis requires liver transplant Liver transplant corrects metabolic defect WILSON’S DISEASE Ceruloplasmin may be normal Behavioral changes Coombs negative hemolytic anemia *Bewer GJ, Yuzbasiyan-Gurkan V. Wilson disease. Medicine (Baltimore) 1992; 71(3):139 KAYSER FLEISCHER RING 46 4/20/2015 CASE 24 A 25 year old woman presents with acute mental status changes and jaundice. She has a history of anorexia and depression. No other past medical history is available. On examination she is lethargic and alert to only person. Kayser-Fleisher rings are not seen on ophthalmologic examination. No stigmata of chronic liver disease are noted on physical exam. Labs: AST 945 IU/L, ALT 765 IU/L, Alk Phos 100 IU/L, T bili 16.8 mg/dL, D. bili 6.4 mg/dL, Hgb 10.4 g/dL, INR 5.2. Ceruloplasmin 17, Acetaminophen level negative. ANA 1:20. Hepatitis A Ab Neg, HCV Ab Neg, 24 hour urine copper 119 mcg. HBV studies are pending. US negative. WHAT IS THE MOST APPROPRIATE NEXT STEP? ER CP io ps y B ... 0% an t at io 0% L iv er D‐ pe ni ci 0% n Re f nd z in c 0% L iv er 0% ni so ne ERCP e a Liver Biopsy E. ra ns pl Liver Transplantation Referral D. T D-penicillamine and zinc C. Pr ed Prednisone B. lla m in A. ACUTE FULMINANT WILSON’S DISEASE Young Age Hemolytic Anemia Psychiatric/Behavioral History Elevated Transaminases with Normal or Low Alkaline Phosphatase Low Ceruloplasmin POOR PROGNOSIS WITHOUT URGENT TRANSPLANT!!! *Ala A, Walker AP, Ashkan K, et al. Wilson’s disease. Lancet 2007 Feb 3;369(9559):397-408 47 4/20/2015 CASE 25 A 28 year old man presents with altered mental status and jaundice. AST 186 IU/L, ALT 92 IU/L, ALP 240 IU/L, total bilirubin 7.2 mg/dL, PT 32.2 sec, INR 3.3. Alcohol was positive in blood and urine. WHICH VALUE IS INCORPORATED INTO MADDREY’S DISCRIMINANT FUNCTION? Pr ot hr 0% re 0% Sc o om a w h l P in in r ia Cr ea t Ar te 0% C 0% a 0% m e Glascow Coma Score Ti Prothromin Time E. om in Ammonia D. Gl as co Arterial Ph C. Am m on i Creatinine B. e A. MADDREY’S DISCRIMINANT FUNCTION Discriminant Function = 4.6 x (Pt’s PT – Control PT) + TBili Value >32 – Treat with Prednisalone 40mg Q Day for 6 Weeks If Renal Failure, Sepsis, or GI Bleed – Treat with Pentoxifilin 300mg BID 30 Day Mortality – 50% Without Treatment *O’Shea RS, Dasarathy S, McCullough AJ, Alcoholic liver disease. Hepatology 2010;51(1):307-28 48 4/20/2015 CASE 26 A 52 year old woman presents with pruritus and fatigue. She complains of a painful skin lesion. On examination, she is obese with a BMI of 35. Labs: AST 68 IU/L, ALT 73 IU/L. ALP 406 IU/L, T Bili 4.2 mg/dL, INR 1.1, Cr 0.8 mg/dL, Glucose 187, total cholesterol 290 mg/dL, AMA negative. Liver biopsy is performed. 49 4/20/2015 WHICH MEDICATION HAS BEEN SHOWN TO IMPROVE SURVIVAL? od i ol 0% 0% s. . . 0% m pr ov e 0% on at e No M ed ic a tio n I 0% Ur s No Medication Improves Survival in this Condition L ip it o r Ursodiol E. en dr Alendronate D. Al Lipitor C. ni so ne Prednisone B. Pr ed A. PRIMARY BILIARY CIRRHOSIS AMA Hallmark but maybe Negative 5-10% of the time Histology – Granuloma, Destruction of Biliary Ductule Complications – Osteopenia, Hyperlipidemia, Pruritus, Fat Soluble Vitamin Deficiency Ursodiol improves transplant free survival Increased risk of Death from Atherosclerosis No Role for Prednisone *Lindor K. Ursodeoxycholic acid for the treatment of primary biliary cirrhosis. N Engl J Med 2007 Oct 11;357(15):1524-29 CASE 27 A 59 year old man is currently listed for liver transplantation for PSC. He had two episodes of cholangitis in last six months requiring IV antibiotics. His MELD score has increased from 15 to 25. His bilirubin has increased from 2.5 to 12.0 mg/dL. He denies any fevers, abdominal pain or vomiting, His cholangiogram reveals a dominant stricture of the common bile duct. 50 4/20/2015 WHAT IS THE NEXT MOST APPROPRIATE STEP? ERCP with Brushings and Biopsy of Bile Ducts and Stenting C. Percutaneous Trans hepatic Cholangiography D. Observation E. Treat for Cholangitis with Antibiotics 0% 0% 0% 0% 0% ER CP L iv w er it h B io B ps ru y sh rc ut in gs an an eo us d. .. T ra ns h ep at Tr .. ea Ob t f se or rv C at ho i on la ng it i s w it. .. Liver Biopsy B. Pe A. PRIMARY SCLEROSING CHOLANGITIS (PSC) Men Greater than Women Strictures throughout the Biliary Tree “Trees in the Winter” “Beads on a String” No Therapy Available Follow for Liver Transplantation and Development of Cholangiocarcinoma in a Dominant Stricture *Chapman R, Fevery J, Kalloo A, Nagorney D et al. Diagnosis and Management of Primary Sclerosing Cholangitis. Hepatology 2010;51(2):660-6780 51 4/20/2015 CASE 28 A 70 year old man presents to the emergency room with hematemesis. He describes early satiety and intermittent nausea. He has lost 10 pounds in the past 4 weeks. He has a history of rheumatoid arthritis. He denies any alcohol, drug use, or tattoos. On examination, he is deeply jaundiced and frail appearing, with no abdominal pain. AST 26 IU/L, ALT 21 IU/L, ALP 253 IU/L, INR 0.7, T Bili 3.1 mg/dL, D Bili 1.9 mg/dL, albumin 3.5 g/dL. ANA positive, AMA negative. Patient undergoes an EGD which reveals non-bleeding fundal gastric varices. No esophageal varices. WHAT IS THE MOST APPROPRIATE NEXT STEP? ER CP 0% 0% bd om en 0% CT A 0% ro GD lo f o gy r B an di ng .. B io ps y 0% Se CT Abdomen its ERCP E. at E D. L iv er Repeat EGD for Banding of Gastric Varices l H ep at Viral Hepatits Serology C. Vi ra B. pe Liver Biopsy Re A. 52 4/20/2015 GASTRIC VARICES Painless Jaundice/Unintentional Weigh loss Pancreatic Cancer Hematemesis with Gastric Varices/Evaluate for Pancreatic Cancer with Splenic Vein involvement Banding of Varices – Poor Results Check CT for Splenic Vein Thrombosis and if Positive, Splenectomy *DeLeve LD, Valla DC, Garcia-Tsao G. Vascular disorders of the liver. Hepatology 2009’49(5):1729-64 CASE 29 A 54 year old male presents for follow up in the office of Cirrhosis with Portal Hypertension. He has had no alcohol intake in 3 years and has been very compliant in follow up and has a strong family support system. He asks “Doc, how’s my liver working and am I ready for a transplant?” 0% 0% AS T 0% in in 0% at AST Cr e Creatinine D. IN R INR C. in Bilirubin B. Bi lir ub A. e ALL OF THE FOLLOWING SEROLOGY WOULD BE HELPFUL IN ANSWERING HIS QUESTION EXCEPT: 53 4/20/2015 MELD Model for End-Stage Liver Disease Based on Logarithmic Calculation of Bilirubin, PT, Creatinine Multiple Calculators available via the Web Consider Liver Transplant consult when MELD is in the mid teens Transplant usually when MELD is in the mid twenties HEPATORENAL SYNDROME Development of acute renal failure in a patient with cirrhosis or fulminant hepatic failure End stage of a sequence of events that reduces perfusion of kidneys Clinical presentation Oliguiria Low urine sodium (often undetectable) Bland urine sediment Systemic hypotension Absence of another cause of renal failure HEPATORENAL SYNDROME Type I 50% reduction of plasma creatinine clearance to a level below 20ml/min or doubling of serum creatinine in less than 2 weeks. Rapidly fatal. Type II Less severe than type I, more indolent and primarily characterized by diuretic refractory ascities. 54 4/20/2015 HEPATORENAL SYNDROME Treatment options Liver transplant. Renal dysfunction improves after transplant. Midodrine (alpha-1 agonist) and Octreotide (somatostatin analog) Midodrine promotes systemic vasoconstriction, octreotide inhibits vasodilitaion of splanchnic vasculature. End result is improved perfusion of kidneys. Norepinephrine Vasopressin analogs TIPS (controversial) Dialysis (only as a bridge to transplant) HEPATORENAL SYNDROME Prevention is key in certain clinical situations SBP – administration of albumin Primary prophylaxis for SBP in patients with low albumin also reduces HRS HEPATOCELLULAR CARCINOMA 5th most common cancer worldwide nearly 1,000,000 new cases annually as of 2007 increasing incidence HBV single most important etiologic factor worldwide Risk increased without cirrhosis HCV and ETOH main risk factors in West 55 4/20/2015 HEPATOCELLULAR CARCINOMA Diagnosis possible without biopsy AFP not sensitive or specific, levels over 200ng/dL highly suspicious for HCC Characteristic appearance with contrasted imaging HCC has arterial blood supply that demonstrates uptake during early arterial phase and contrast washout in the delayed venous phase Biopsy is warranted in a liver mass larger than 2 cm without typical radiographic findings and no elevation in AFP HEPATOCELLULAR CARCINOMA Early Arterial Phase CT heterogeneously enhancing mass 4-5 cm Portal Venous Phase CT Decreased enhancement, isoenhancing with liver FINAL THOUGHTS ON THE LIVER Always give your patients with Cirrhosis and Gastrointestinal Bleeding Antibiotics because they improve outcomes Serum Ammonia Levels have no role in managing patients with Hepatic Encephalopathy – Clinical Diagnosis Always remember precipitating causes of Encephalopathy including Gastrointestinal Bleeding, Sedating Drugs, Infection, and Medical NonCompliance 56 4/20/2015 FINAL THOUGHTS ON THE LIVER Remember Risk Factors for Hepatitis C including IV Drug Use, Nasal Cocaine Use, Blood Transfusion prior to 1990 Poor Transmission of Hepatitis C by Sexual Intercourse Doubt Treatment will be asked but Oral Anti Replicase Agents have taken the place of older therapies Remember Hepatitis B can be Reactivated by Chemo Therapy or Immunosuppression for Inflammatory Bowel Disease FINAL THOUGHTS ON THE LIVER Remember there is no Chronic form of Hepatitis A but you can get a relapsing Cholestatic Hepatitis Remember the majority of Hepatitis B infections are self limited where as the majority of Hepatitis C infections are Chronic Remember the risk of Cirrhosis from Hepatitis C is approximately 20% after 20 years duration. Alcohol can accelerate this process GOOD LUCK ON THE EXAM!!! Please feel free to contact me with any questions prior to the Exam. 57