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GI Board Review with Questions (Part Two): Viral Hepatitis, Acute Upper GI Bleeding, Variceal bleeding, Lower GI bleeding, Complications of cirrhosis, Diarrhea


    Viral Hepatitis

    Hepatitis B 
    Importance of Hepatitis B in pregnancy is related to its role in the perpetuation of chronic infection through vertical transmission
    • Maternal-fetal transmission of HBV is responsible for most cases of HBV worldwide
    • +HBe ag have more circulating virus and higher rates of perinatal transmission (as high as 90% transmission if untreated)
    • Antiviral Rx recommended starting week 32 if HBV DNA > 200,000 IU/ml

    Prevention: infant should receive hepatitis B immunoglobulin at birth and vaccine during 1st day of life, one month, and six months

    Hepatitis C
    vertical transmission uncommon
    Risk factors
    • HIV coinfection
    • Hx of IV drug abuse
    • Maternal viremia of > 106 copies/ml

    Transmission rates unaffected by mode of delivery

    Acute Upper GI Bleeding

    • Incidence: 36-100 per 100,000 persons
    • 40% > 60 years old
    • Self-limited in 75-80%
    • Endoscopic hemostasis done in 25% Mortality
    • Overall: 14% (10-36%)
    • Admission for GI bleed: 11 % mortality
    • Gl bleed in the hospitalized: 33 % mortality

    Causes of Upper GI bleeding


    Severity Assessment of Upper GI bleeding
    • Agitation
    • Hypotension
    • Pallor or Hemoglobin < 8 g/dL
    • Tachycardia or Bradycardia (vagal)
    • Orthostasis

    Management of Upper GI bleeding
    • Oxygen supplementation
    • Central line or two large bore needles
    • Resuscitate first with "0.9% NaCl" or "Lactate Ringer" solution
    • Start blood transfusion if needed: goal Hgb is 7-8 g/dL, Exception: Consider transfusion when Hgb < 8 g/dL in: Acute coronary syndrome, Exsanguination: Hypotension/tachycardia that indicates intravascular depletion with artificially high Hgb.
    • Start PPl therapy
    • Gl consult for Endoscopy
    • Surgery consult and/or IR consult
    • If cirrhosis is known or suspected: Antibiotics: Ceftriaxone or Ciprofloxacin x 7 days. Octreotide (or Somatostatin) drip

    Variceal bleeding

    • Varices form at rate of 5-15%/year
    • About 30% will bleed at some time
    • Bleeding only if HPVG >12mm Hg; "clinically significant portal HTN" is >/ = 10 mm Hg
    • Mortality from variceal bleed = 15-30% / episode If untreated, 70% will die within a year.
    • In-hospital mortality: 40 % (due to continuous bleed, re-bleed, advanced disease, infection, HRS)
    • Mortality after 2 week survival: 52 % at 1 year

    Lower GI bleeding

    • Incidence: 20/100,000 persons
    • Mortality: 3.6% (23% if starts in hospital)
    • Mean Age: 63-77
    • Source of Hematochezia: 76% colon, 11% above Ligament of Trejtz, 9% small bowel, 6 % unknown

    Etiology of Lower GI Bleeding
    • Diverticulosis: 33%
    • Colon Ca or polyps: 19%
    • Colitis (IBD, infectious, ischemic, radiation, vasculitis, etc.): 18%
    • Angiodysplasia ( AVM): 8%
    • Other intestinal lesions (post-polypectomy, Aorto- enteric fistula, stercoral ulcer, etc.): 8%
    • Ano-rectal: 4%
    • Unknown: 16%

    Diverticular Bleed
    Occurs in 3-15% of patients with diverticulosis
    Causes 30-50% of massive hematochezia.
    Cause: Erosion of artery in dome of diverticulum.
    Presentation: Painless maroon or red bleed
    Location: Right colon 50-90% (< 25% of tics are in this region) Course:
    • Persistent bleed in 20%
    • Stops spontaneously in 75-80%
    • 25% re-bleed @ 4y

    • Endoscopic treatment; if fails:
    • Arteriography + Intra-arterial vasopressin is successful in 90%.
    • Surgery: Persistent bleeding or multiple Re-bleeds

    Angiectasia of Colon
    Prevalence in screening colonoscopy is ~ 1%
    Multiple in 40 -60%
    Frequency of bleed
    • Less than 10% of angiectasia patients bleed
    • Once they bleed, up to 50% re-bleed

    Age: 2/3 are > 70 y old.
    • acute hemorrhage in 45%
    • low grade blood loss in 55%

    • Octreotide ggt, Endoscopic therapy
    • Long-acting octreotide ( Sandostatin LAR depo) for recurrent bleeding
    • Iron supplementation, PRBC

    Ischemic Colitis
    • Clinical features plus imaging
    • Flex-Sig or colonoscopy - Mucosal inflammation, ulcers

    • IV fluid resuscitation + bowel rest, and antibiotics
    • Improve oxygenation and cardiac output
    • Anticoagulation + hypercoagulability work-up for acute mesenteric vein thrombosis

    • most improve in 1-2 days, and resolve in 1-2 weeks.
    • 20% develop chronic ischemic colitis with strictures, recurrent bacteremia, protein loosing enteropathy, bloody diarrhea and/or weight loss. May need resection

    A 65 yr old male with end stage heart failure and atrial fibrillation after multiple prior Mls has a continuous flow left ventricular assist device placed. He is discharged on ASA, omeprazole, digoxin and coumadin but is readmitted 3 months later with symptomatic anemia (hgb of 6.8, MCV of 75) and painless bright red rectal bleeding. His platelet count is 196k and his INR is therapeutic (2.5).

    Which one of the following is the most likely source for his bleeding:
    A. Ischemic colitis
    B. Peptic ulceration
    C. AVMs of the bowel
    D. Congestive hepatopathy and portal hypertension

    C) AVMs of the bowel

    A 72-year-old man on 81 mg ASA for secondary prophylaxis after an MI 2 years ago (also taking a B-blocker and a lipid lowering agent) presents with a hemodynamically significant upper GI bleed. His ASA is held and he undergoes urgent EGD in the presence of an IV PPI continuous infusion to reveal an actively bleeding gastric ulcer. Hemostasis is achieved with epinephrine injection and placement of two clips.

    Which of the following statements regarding his ASA therapy is correct?
    A. His ASA therapy should not be restarted
    B. His ASA should be restarted after repeat EGD documents healing of the ulcer in 6-8 weeks time
    C. His ASA should be restarted in 5 days
    D. He should be switched to coumadin instead of ASA

    C. His ASA should be restarted in 5 days

    A 46-year-old male presents to the emergency department with a 24 hour history of melena and dizziness. He was well until he noticed significant shortness of breath after his daily 5 mile jog. He has a history of plantar fasciitis but takes no prescription meds. He drinks 2 beers a day. Examination reveals a diaphoretic, pale male in mild distress. EGD reveals multiple erosions in the pre-pyloric area and clean based duodenal bulb'ulcer are identified. A rapid urease biopsy of the antrum and body are both H. pylori-negative and additional specimens are sent for histology. He has no further bleeding and is discharged on iron supplementation and a PPI. The pathology comes back later demonstrating foveolar hyperplasia but no gastritis.

    The most likely etiology of his ulcer disease is:
    A. Alcoholic gastropathy
    B. Undeclared NSAID use
    C. Unrecognized H. pylori gastritis
    D. Ischemic gastropathy

    B. Undeclared NSAID use

    Complications of cirrhosis

    • Ascites
    • Varices
    • Encephalopathy
    • Hepatocellular Carcinoma
    • Hepatorenal syndrome and hyponatremia
    • Hepatopulmonary syndrome/Portopulmonary hypertension

    #1 complication of cirrhosis
    50% cumulative probability of developing ascites 10-years after diagnosis of cirrhosis
    50% mortality 2 years after developing ascites
    Portal hypertensive ( SAAG > 1.1)
    • Cirrhosis
    • Heart Failure
    • Budd-Chiari
    • Portal Vein thrombosis
    • Alcoholic hepatitis
    • Acute liver failure
    • Sinusoidal obstructive syndrome or veno-occlusive disease

    Non-Portal hypertensive ( SAAG < 1.1)
    • Peritoneal carcinomatosis
    • Biliary ascites
    • Pancreatic ascites
    • Nephrotic syndrome
    • Chylous ascites
    • Serositis
    • TB
    • Myxedema

    TIPS (Transjugular intrahepatic portosystemic shunt) for refractory ascites ( nonresponse to maximum doses of diuretics (furosemide 160 mg/d spironolactone 400 mg/d) or hyponatremia or AKI)
    • MELD<18, t bili< 3
    • No pulmonary HTN (ECHO)
    • No history significant encephalopathy


    Contraindications to Placement of TIPS
    • Primary prevention of variceal bleeding
    • Congestive heart failure
    • Pulmonary hypertension (severe)
    • Uncontrolled infection/sepsis
    • Unrelieved biliary obstruction
    • Multiple hepatic cysts

    • HCC (particularly if central)
    • Portal vein thrombosis (cavernous transformation)
    • MELD>18, Bili>4, INR>5
    • Obstruction of all hepatic veins

    Spontaneous bacterial peritonitis
    Occurs in 20% of cirrhotics with ascites
    15% mortality
    50% of patients with SBP are bacteremic
    • >250 PMN ascites or + gram stain or culture

    Treatment of SBP
    • IV cefotaxime, amoxicillan/clavulanic acid, or quinolone
    • IV albumin (1.5 g/kg day 1, 1 g/kg day 3)
    • Avoid therapeutic paracentesis/IV contrast or aggressive diuresis
    • Repeat diagnostic paracentesis in 48 -72 hrs if no clear clinical response
    • If clinically responding or decrease in PMN's by 25% on follow up paracentesis can switch to oral therapy
    • Outpatient treatment of SBP: no nausea, vomiting, fever, renal dysfunction or encephalopathy
    • Duration of treatment: 5-7 days

    Hepatic Encephalopathy
    • Lactulose po/tube
    • Lactulose retention enema: 300 cc lactulose, 700 cc H20, Retain with balloon for 30 minutes
    • Rifaximin 550 mg po bid
    • Zinc
    • L-carnitine 990 mg po tid
    • Always look for possible causes: dehydration, infection, Gl bleed, medication non-compliance
    • Keep in mind other possible causes for AMS

    A 21 year old female is hospitalized with jaundice, myalgias, and malaise. She denies abdominal pain or fever. On exam, she is jaundiced but has no stigmata of chronic liver disease. Her mental status is clear. She has no history of new drug use or alcohol abuse, but admits to regular cocaine snorting and intravenous use. She denied OTC drug use, including NSAID's or acetaminophen. Her laboratories include:
    • ALT 310 U/L, AST 251.
    • HBV core IgM neg
    • TBili 1.0 mg/dL
    • HBs ag - neg
    • INR 1.2
    • Ferritin 1300 ug/ml ANA - normal
    • Alk phos 134
    • HAV Ig M - neg
    • protein 7.5
    • HCV Ab neg
    • Albumin 3.4
    • Acetaminophen level is normal

    What is the most likely diagnosis?
    A. Hemochromatosis
    B. Serology-negative hepatitis B
    C. Autoimmune hepatitis.
    D. Acute hepatitis C

    D. Acute hepatitis C

    A 27 year old female state she ingested two handfuls of extrastrength acetaminophen tablets after an argument with her boyfriend, then brought herself to the ER for evaluation 6 hours later. Her exam is normal. Her labs are notable for:
    • AST 265 U/L (normal <40 IU/L)
    • ALT 370 U/L (normal <40 IU/L)
    • TBili 1.0 mg/dL
    • INR 1.2
    • Alk phos 134
    • protein 7.5
    • Albumin 3.4
    • Acetaminophen level 45 ug/mL

    What is the appropriate management of this patient?
    A. Discharge from the ER with follow-up because her Rumack normogram does not predict hepatotoxicity
    B. Immediate N-acetylcysteine
    C. Transfer to a liver transplant center
    D. Immediate PO charcoal

    B. Immediate N-acetylcysteine

    A 52 y/o male with decompensated cirrhosis from hepatitis C presents with severe ascites. He is currently taking furosemide 120 mg oral daily and spironolactone 200 mg oral daily and lactulose 30 cc three times a day. Despite his adherence to lactulose he gets confused. His serum creatinine is 2.1 mg/dL, serum sodium 125 mmol/L, total bilirubin 4.2 mg/dL, and INR 1.9 seconds.

    Which therapy is most appropriate?
    A. Increase furosemide to 160 mg daily and spironolactone to 300 mg daily
    B. Serial large volume paracentesis with intravenous albumin replacement
    C. Transjugular intrahepatic portosystemic shunt
    D. Abdominal catheter

    B. Serial large volume paracentesis with intravenous albumin replacement

    A 43 year old man is hospitalized with jaundice. He has been drinking 1 pint of whisky daily for the past four months. He denies other risk factors for liver disease. Examination reveals a blood pressure 110780, pulse 110; respirations 16 temperature 37 degrees. He is jaundiced. Abdominal examination reveals a liver 4 Finger breadths below right costal margin, a palpable spleen tip, but no shifting dullness.

    Laboratory studies:
    • WBC 17,500
    • Bilirubin 7 mg/dL
    • AST 210 U/L
    • ALT 69 U/L
    • AP 140 U/L
    • PT 14 seconds
    • Ferritin 660 u/L
    • Discriminant function 25

    A liver biopsy shows steatohepatitis, hepatocyte ballooning, and Mallory's hyaline.

    In addition to recommending alcohol cessation, which of the following is the most appropriate treatment?
    A. Prednisolone
    B. Pentoxifylline
    C. Prednisone and pentoxyphylline
    D. Adequate nutrition

    D. Adequate nutrition

    You admitted a patient to the intensive care unit with hematemesis who has a history of cirrhosis. He is not on home medication. His physical exam shows BP 90/60 mmHg, HR 110, he has scleral icterus, on abdominal exam he has ascites, splenomegaly. Labs reveal hemoglobin 11.1 g/dL, platelet count 78,000, WBC 5,200, creatinine 1.6 mg/dL, T bili 1.6 mg/dL, AST 68 U/L, ALT 45 U/L, INR 1.4. albumin 3.4 g/dL. ER had consulted GI. EGD reveals large varices and 6 varices are banded.
    He is started on intravenous octreotide and pantoprazole

    Which of the following should be recommended next?
    A. Transfuse PRBC 2 units
    B. Transfuse Fresh frozen plasma 2 units
    C. CT scan abdomen with IV contrast
    D. Ceftriaxone

    D. Ceftriaxone

    A patient with new-onset ascites but no known history of liver disease has the following portal pressures obtained at Transjugular liver biopsy: wedged hepatic vein = 25 mmHg; free hepatic vein = 6 mmHg.

    The most likely cause of this patient's ascites is:
    A. Right heart failure
    B. Extrahepatic portal vein thrombosis
    C. Liver cirrhosis
    D. Budd-Chiari syndrome

    C. Liver cirrhosis


    A 38 year-old alcoholic presents with new-onset ascites. Diagnostic paracentesis reveals a cloudy fluid with total protein of 1.5 g/dl, SAAG of 1.6 g/dl, and cell count 350 WBC (9% PMN).

    The most likely etiology for his ascites is:
    A. Alcoholic cirrhosis
    B. Cardiomyopathy
    C. Lymphoma
    D. Peritoneal tuberculosis

    A. Alcoholic cirrhosis

    A 64 year-old male presents for evaluation of shortness of breath and abdominal distension. He has a past medical history of diabetes and hypertension. Physical exam shows a distended abdomen with flank dullness and hepatomegaly. An ultrasound confirms the presence of ascites and patent hepatic and portal vein and liver span of 20 cm. Blood work reveals AST 60 U/L, ALT 50 U/L, total bilirubin 1.7 mg/dL, alkaline phosphatase 148 U/L, platelets 180,000, albumin 3.0 mg/dL, creatinine 1.8 mg/dL. A paracentesis is performed and reveals a total nucleated cell count of 180, albumin 1.3 mg/dL, total protein 3.1 g/dL

    Which of the following is the next best step?
    A. Intravenous furosemide
    B. Abdominal CT with intravenous contrast
    C. Echocardiogram
    D. Liver biopsy

    D. Liver biopsy


    Small and large intestine absorb 99% of 10 liters of fluid that traverse through the gastro-intestinal tract daily
    • Jejunum 6 liters
    • lleum 2.5 liters
    • Colon1.5 liters

    Water is absorbed following osmotic forces

    • < 14 days in duration
    • 450 000 hospitalizations/year

    • 14 to 30 days

    • > 30 days
    • 3 - 18 % of the adult population (~5%)

    Classification - Pathophysiologic
    • Osmotic /Malabsorption- osmotic load in the intestine resulting in retention of water in the lumen
    • Secretory - excess secretion of electrolytes and water into the intestinal lumen
    • Inflammatory - exudation of fluid and protein from the intestinal mucosa
    • Motility - rapid transit through the colon due to autonomic dysfunction, rapid small intestine transit, and/or colonic irritability

    Acute diarrhea
    Infectious - commonest cause
    Most common infections are viral
    < 6 hr after ingestion: preformed toxin
    • Staphylococcus aureus, Bacillus cereus

    8 - 14 hours
    • Clostridium perfringes

    >14 hours
    • Viral/bacterial

    Bloody stool and fever
    • Salmonella, Shigella, Campylobacter
    • Viral
    • C. difficile, Entamoeba histolytica

    Osmotic Diarrhea
    • If malabsorbed nutrients or non-absorbable solutes are ingested, fluid will enter the intestine to reach iso-osmolarity. Normally, most of the stool osmolarity comes from its electrolytes (Na, K, corresponding organic anions)
    • Osmolar gap = 290 - 2[Na +K]; Normal < 125 mOsm (usually < 50 mOsm)
    • Features of Osmotic Diarrhea: - Osmolar gap > 125 mOsm

    • Osmolar load: PEG, Mg salts, Na Phosphate, sorbitol, mannitol, lactulose, xylitol
    • Malabsorption: mucosal damage (sprue, infections), disaccharidase deficiency, bacterial overgrowth, pancreatic insufficiency, short bowel, IBD, lymphangiectasia, etc.

    Secretory Diarrhea
    • Due to inhibition of ion (Na, K, Cl, HCO3) absorption, stimulation of ion secretion, or both.
    • May affect small bowel, colon, or both; in small bowel disease, the amount of fluid presented to the colon exceeds its maximal absorption capacity (5 L)
    • Osmolar gap < 50 mOsm

    • Drugs: bisacodyl, senna, aloe, ricinoleic acid, misoprostol, colchicine, etc.
    • Foods: tea, coffee, seafood toxins (ciguatera, scombroid, paralytic or neurotoxic shellfish poisoning)
    • Bacterial toxins: S. aureus, C. perfringes, C. botulinum, B. cereus

    • Bacterial: V. cholerae, Toxigenic E. coli, C. jejuni, Y. enterocolitica, C. difficile
    • Endogenous laxatives: bile acids, long-chain fatty acids
    • Hormone-producing tumors: VIPoma,, carcinoid, glucagonoma mastocytosis

    Inflammatory Diarrhea
    Enterocyte damage or death, with minimal or severe inflammation; can cause malabsorption or secretion

    • Infections: E. coli, salmonella, shigella C. jejuni, Y. enterocolitica, M. avium complex, Whipple dz, rotavirus, Norwalk, HIV, giardia, cryptosporidium, isospora, cyclospora, ascaris, trichinella, bacterial overgrowth, tropical sprue.
    • Cytostatics: chemotherapy, radiation.
    • Hypersensitivity: food allergy, celiac sprue, milk or soybean hypersensitivity, eosinophilic gastroenteritis ,nematodes.
    • Autoimmune/ idiopathic: microscopic colitis, ulcerative colitis, Crohn's disease

    Altered Motility
    • Due to autonomic dysfunction, rapid small intestine transit, and/or colonic irritability.
    • Post-surgical: Vagotomy, gastrectomy, cholecystectomy
    • IBS
    • Hyperthyroidism
    • Most diarrheal disorders have more than one pathophysiologic component

    Historical clues to diagnosis
    Stool volume:
    • Small (< 250 g + tenesmus, frequency, urgency, mucus or blood: suggest recto-sigmoid involvement.
    • Large > 400 g, watery, minimal urgency, no tenesmus, little mucus: suggest SB or proximal colon origin, secretory diarrhea.
    • Large > 400 g, foul smelling, greasy, minimal urgency, no tenesmus: suggest SB origin with malabsorption

    • Periumbilical or RUQ, crampy, with borborigmi: small bowel or asc. colon.
    • Hypogastric, RLQ, or LLQ, aching, with tenesmus: rectosigmoid

    • mucosal invasion (salmonella, campylobacter)
    • IBD, neoplasia
    • ischemia
    • cytotoxin (EHEC, C. difficile, Shigella, Klebsiella oxytoca)

    Effect of fasting ( 48 hr):
    • Stops: osmotic or allergic
    • Continues: secretory or inflammatory

    Histologic clues
    • Foamy macrophages: Mycobacterium avium intracellulare and Whipple's disease: a) Acid-fast bacilli: MAC, b) No acid-fast bacilli: Whipple's disease
    • Flask-shaped ulcers: Entamoeba histolytica
    • Owl's eyes intranuclear inclusions: CMV infection
    • Ground-glass nuclei with Cowdry A intranuclear inclusions: HSV infection

    Historial clues to etiology of diarrhea
    Nocturnal Diarrhea: suggest organicity
    Food ingestion:
    • Undercooked Poultry: salmonella, campylobacter, shigella.
    • Ground beef, unpasteurized juice: Entero-Hemorrhagic E. coli.
    • Pork: tapeworm.
    • Seafood/shellfish: v. cholerae, v. vulnificus, V. parahemolyticus, salmonella.
    • Cheese, milk: listeria.
    • Eggs, unpasteurized orange juice, raw milk : salmonella.
    • Mayonnaise & cream pies: S. aureus & clostridium.
    • Fried rice: B. cereus

    Clostridium difficile
    • Complications: toxic megacolon requiring colectomy
    • Risk high in >65 y/o, immunosuppression & hospital acquisition.
    • Risk factors for complicated nosocomial PMC ( pseudomembranous colitis): WBC > 20K, Creat > 2 mg/dL
    • Mortality higher in patients with “hypervirulent strain”
    • Mortality due to "Fulminant” PMC: 50 % (most within initial 48h)

    Treatment of multiple relapses/recurrences
    • Vancomycin PO 125mg q6h x10d, then BID x7d, then daily x7d, then every other day x21d
    • Bezlotoxumab 10 mg/kg IV X 1 may be used as an adjuvant therapy for recurrence prevention
    • Fecal Microbiota Transplant (FMT)

    You are the physician in a cruise ship in the Caribbean. At midnight there is an "oriental buffet” At 3 am a passenger comes to your office complaining of abdominal cramps, nausea, vomiting and diarrhea; over the next 2 hours another 72 passengers are waiting to be seen.

    What is the most likely cause of the illness?
    A. Clostridium perfringes
    B. Enterotoxigenic E. Coli
    C. Bacillus cereus
    D. Rotavirus
    E. Enterohemorrhagic E. Coli

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