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Conferences and Medical Updates

Arcadia 2015 – notes from Lindsey F.

GASTROENTEROLOGY OBJECTIVES

  • Retroperitoneal Organs: SAD PUCKER (Supra renal, adrenal glands, aorta, IVC, Duodenum, Pancreas, Ureters, Colon, Kidneys, Esophagus and Rectum)
  • GI Tract Histology
    • Mesentery and mesothelium
    • < >Myenteric plexus
    • Outer Longitudenal
    • Inner circular
    • Submucosal plexus
    • < >Muscularis mucosa and then mucosa
  • Basal Frequencies:
    • Stomach 3 waves a minute
    • Duodenum 12 waves a minute
    • Ileum 8-9 waves a minute
  • The Pectinate Line
    • Above pectinate lines – Int. hemorrhoids
    • Below pectinate line – ext.hemorrhoids . Pain from pudendal nerve
    • Anal fissure – The Ps- pain while pooping, posteriorly poor perfusion, paper
  • Esophageal Disorders
    • < > a form of indigestion felt as burning in the chest, caused by acid regurgitation into the esophagus. Dysphagia- Difficulty swallowing. Can occur in the mouth area, as well as in the esophagus.
      • Can occur for solid or liquid food.Favors motility disorder, candida infection.
      • Can be progressive or intermittent.
        • Progressive: Solid to liquid suggests mech. Obs.
        • Intermittent: Suggests Schatzkis ring, EE, web
      • Tests- EGD, Ba swallow, motility studies, Video Ba swallow
        • Completed by speech therapists
    • < > Painful swallowing. Examples: Herpes ulcer, CMV, primary HIV ulcer.
  • Oropharyngeal dysphagia- Food may go to nose or they start choking. Patients often point to area of problem
    • Can present as recurrent pneumonias
    • Can occur after CVA, parkinsons
    • May need Video Ba swallow
    • Treatment usually PEG tube insertion
    • Can present as recurrent pneumonia
      • Dysphagia, all pneumonias are aspiration in reality
      • Microscopic aspirations
      • Commonly infected by anaerobic species.
        • Screen Shot 2014-10-19 at 5.07.49 PM.pngTreated with clindamycin, metronidazole, PCNs (amox).
    • PEG tube – percutatneous endoscopic gastronomy, get food through tube in stomach,
  • Esophageal Atresia
    • Three types:
      • Pure EA (gaseless abdomen)
      • Pure TEF H type
      • EA with distal TEF
      • Cyanosis from laryngospasm
    • S/S drooling, choking and vomiting
  • Congenital Pyloric Stenosis
    • Hypertrophy of the pylorus
    • Olive mass in epigastric region
    • Non bilious projectile vomiting
    • 2-6 weeks after birth
    • Incidence 1/600
    • Usually males, first born
  • < >- a condition when the lower esophagus spincter (LES) fails to relax, prohibiting food to ender stomach.  Characteristic feature is failure of LES to relax and aperistalsis of distal esophagus.
  • Can be primary or idiopathic or secondary.
  • Secondary causes include malignancies ( breast, pancreatic, prostate, gastric), infections (Chagas disease) etc
  • Occurs in 1 in 100000 cases
  • Results from idiopathic post ganglionic denervation of distal esophagus.
  • Presents as dysphagia, chest pain, weight loss, aspiration pneumonia
  • Has characterstic Ba swallow appearance and manometric studies
  • < >Botox injections
  • Endoscopic dilatations
  • Hellers myotomy (open or laproscopic)
  • It is known as POEM. (per oral endoscopic myomectomy)
  • Motility Disorders
    • Poorly defined
    • Some may correlate with chest pain
    • Treatment is with smooth muscle relaxants but no control data
    • Some of these disorders may respond to NTG.
  • Eosinophilic esophagitis- Under recognized disorder in which an allergic atopic reaction occurs in the esophagus
    • Etiology:
      • More common in males, pediatric age group, mostly presents as dysphagia and food impaction. No cases in Africa. Newer, increasingly recognized by physicians, common in teens, allergic reaction to food products that causes symptoms in the esophagus.
      • Commonly caused by GERD, PPI response, Chrohn disease, and rarely pemphigus.
    • Sx:
      • EGD: Vertical mucosal lines. Multiple rings in esophagus. White papules. Fragile esophagus. Loss of vascular pattern. Needs multple biopsies (10-15 eosinophils per HPF).
      • History of dysphagia and episodes of food impaction. Heartburn may be present.
    • Dx:
      • History of atopic dermatitis often present as well as other allergic conditions.
      • Few have elevations in IgE levels
      • Endoscopy and biopsy will reveal diagnosis.
        • White exudates or papules, red furrows, corrugated concentric rings, strictures
    • Tx:
      • Treatment includes avoiding certain foods (avocado, shellfish, peanuts, honey, milk, soy, egg, wheat), allergy testing.
      • Medications include Fluticasone and Budesonide. Overlap with GERD and PPI work too.
        • Steroid inhalers may be useful
      • Elemental diet milk eggs, soy, wheat peantus tree nuts and shellfish – Six food elimination diet diet 80% effective. Custom diet and FODMAP diet are other options. Ciclosonide and Reslizumab in the future?
  • Esophageal Ulcers
    • < >< >Infections like Herpes (can occur in non immunocompromised individuals, Rx acyclovoir), HIV (the HIV virus itself, Rx steroid), CMV (low CD4 count, Rx gancylovoir).
    • Medications like steroids, NSAIDS, fosamax, KCl, Doxycycline, This is called pill esophagitis
    • Crohns dis
    • < >Candida Esophagitis
      • White cheesy material in the esophagus.
      • Usually occurs in immunocompromised patients (HIV, cancer), Diabetics.
      • Rx Diflucan
    • Esophageal Tumors:
      • < >Lipoma, Pappiloma and leiomyomas.
    • < >Squamous cell
    • < >Squamous Cell Carcinoma of the Esophagus
      • Proximal 2/3 of esophagus
      • More in men
      • More in African American population
      • Risk factors are cigarette smoking, alcohol, severe iron def (Plummer vinson syndrome), Celiac sprue, tylosis, lye stricture, scleroderma, achalasia,
      • RF: AABCDEFFGH
        • Achalsia, alcohol, Barrett,smoking, diverticuli,esophageal web, familial, fat,GERD,Hot liquids
    • < >Related with GERD and Barretts esophagus.
  • Esophageal CA:
    • Survellience indicated for Barretts
    • Survellience indicated for patients with tylosis, lye ingestion, achalasia.
    • Staging is done with CT and EUS
    • Use the TNM classification
    • Stage 1 and 2 treatment is surgery (either cancers)
    • Palliation can be achieved with laser debulking, stents and dilatation, radiation
    • Newer techniques such as EMR can help treat esophageal cancers too! It is done endoscopically – endoscopic mucosal resection
  • Barretts Esophagus
    • Squamous epithelium is replaced by columnar intestinal epthelium
    • Occurs in 6-12% of patients undergoin EGD for GERD and 1% of unselected patients
    • Short segment or Long segment (more than or less than 3 cm)
    • < >Risk of cancer is 0.1% per patient per year for no dysplasia, 19% with HGD and 3% with LGD.
    • Treatment is generally surveillance.
    • Surveillance interval is determined by presence of dysplasia.No dysplasia 3 years, low grade dysplasia 1 year, high grade dysplasia (either surgery, APC, EMR after confirmation or repeat in 1-3 months).
    • If you get 200 patients with barretts, 1 will get cancer in any given year, not common
    • PPI does not get rid of barretts
    • BE risk factors include obesity, smoking, GERD, medications such as bisphosphonates, NTG, B agonists, Hp infection.
    • Green leafy vegetables increases nitrous oxide in LES and higher chance of BE
    • PPI can cause regression of Barretts
    • Surgery with fundoplication does not get rid of the existing Barretts
    • Treatment options include PDT (photodynamic therapy), EMR (endoscopic mucosal resection), thermal ablation.
    • RFA (radiofrequency ablation) 98% cure rate.
    • < >Esophageal webs and strictures
      • Thin mucosal structures that may compromise the lumen
      • Can be congenital
      • Distal rings are often Schtazkis ring
      • Proximal are often webs
      • Usually present as dysphagia.
      • Schatzkis ring can present as “steakhouse” syndrome
      • Dysphagia occurs when lumen is 13mm or 39 Fr or less
      • Can be subtle and missed on EGD.
      • Ba swallow might pick up subtle strictures
      • Rx is dilatation (Schatzkis ring may require dilatation upto 50 Fr).Be careful of dilatation in Eosinophilic esophagitis
      • Proximal web – can be associated with iron def.(Plummer Vinson syndrome or Paterson-Kelly syndrome)
      • Dilatation can be done in 3 ways:
        • Balloon Dilatation
        • < >< >The later two is called bouginage.
  • Gastroesophageal reflux disease (GERD)- a condition which develops when the reflux of stomach contents causes troublesome symptoms and/or complications
    • Essentials of Diagnosis:
      • Heartburn, which may be exacerbated by meals, bending or recumbency
      • Typical uncomplicated cases do not require diagnostic studies
      • Endoscopy demonstrates abnormalities in one third of patients.
    • Risk Factors:
      • Alcohol, caffeine, obesity, smoking, poor gastric emptying, impaired esophageal peristalsis, impaired salivation, hypersecretion of gastric acid (Zollinger-Ellison Syndrome)
    • Pathophysiology:
      • Sphincters relax too much, which allows the contents of the stomach to move up.
      • Primarily a motility disorder of the lower esophageal sphincter (LES) with abnormality of the tLESR.
    • < > Cough at night, wheezing, acidic taste in mouth, hoarseness, chronic sore throat. ALARM SYMPTOMS: weight loss, occult/overt GIB, unresponsive to PPI. Heartburn, chest pain, dysphagia (from motility problem), regurgitation, waterbrash (extra salivation), post-prandial fullness, bloating, satiety, nausea.
    • Chest pain is aypical, regurgitation, relief with antiacids, associated with meals,
    • Extra-esophageal: hoarseness of voice, cough, asthma, Sandifers syndrome, rampant cavities, laryngitis.
      • 3 Most common causes of Cough: Asthma, GERD, Sinusitis. ACEi can also cause cough.
      • Sandifer’s Syndrome– patients present with SCM muscle spasm.
    • Laryngitis-those with vocal cord granuloma is the only read GERD or LPR. Other findings such as erythema, cobble-stoning are non-specific.
      • Sx such as throat clearing, hoarseness, cough, globus, sore throat (no advantage of PPI over placebo)
    • < >- Non-erosive esophageal disease. Tx:
      • Antacids – Mg containing antacids causes diarrhea.Aluminium containing antacids cause constipation.Calcium containing is a reasonable option in many situations
      • Lifestyle Modifications:
        • Decrease alcohol consumption, decrease caffeine, decrease acidic foods (tomatoes, onions), avoid medications that decrease LES tone:
          • CCB, BB, Nitrates, anticholenergic drugs.
        • Weight loss, tobacco cessation, avoidance of meals 3 hours before bed, elevation of head of bed.
      • Acid suppressive medications (PPIs most effective), but the stomach contains more than just acid. Dietary changes (avoid fried food), small frequent meals, weight reduction, blocks, do not lie down within 2 hours after meals.
      • PPI- Block a common pathway to the production of acid, Prodrug. Most effective when taken 30 – 60 min before breakfast or dinner. Life long treatment.Long term side effects of PPI may include osteoporosis, Pneumonias, Mg and C diff infections
      • < >- magnesium and aluminum together, which causes diarrhea and constipation, thus counteracting each other. Treatment of H. pylori is counterintuitive to tx. This could increase the acid production, which increases symptoms.
      • Some benefit with using zinc loszenges.
        • Calcium containing is a reasonable option in many situations
      • H2 blockers – quicker action but limited efficacy.Causes tachyphylaxis.
      • < >< >  Can be done open or laproscopically.  The wrap can be complete or incomplete.  Often known as Nissen fundoplication. Death rate is 1% and life threatening complications is 2-3%If medicines fail, surgery will not work.
      • Currently, there is no endoscopic surgery that is widely accepted.
    • Treatment Failures: non-compliance, not taking medications at the right time, increase to bid.
    • Notice that GERD is a motility disorder but there is no prokinetic drug available!
    • Baclofen has been tried in select cases.Side effects include fatigue and sleepiness.
    • Newer drug is Arbaclofen
    • Reglan has unacceptable side effects and is ineffective.
  • < >Esophageal strictures, hemorrhage, Barretts esophagus, adenocarcinoma
  • Complications can occur in asymptomatic patients
  • Borhaave Syndrome– esophageal rupture from violent retching. This is a tear in all the layers of the esophagus. Treatment is surgery or stenting.
  • Plummer Vinson Syndrome
    • Dysphagia from esophageal webs, Iron def and glossitis (DIG)
    • Stomach Disorders
    • < >< >Appears endoscopically as erosions, usually painless and little inflammation
    • Can occur from NSAID use and Pg depletion
    • Other risk factors include shock, ventilator dependent, Coagulopathy, multiorgan failure.
    • Prophylaxis with carafate, PPI, maintaining pH >5.
    • IV PPI is associated with retinopathy!
    • PPI is associated with a higher incidence of Pneumonias, Mg depletion, osteoporosis and C diff
  • NSAID related
  • < >H pylori
    • First discovered by an Australian gastroenterologist named Barry Marshall.
    • It is found in 96% of DU cases and 75% of gastric ulcers
    • Can also lead to gastric adenocarcinoma and MALT tumor (malignant) of the stomach.Atrophic gastritis from Hp can lead to iron def. anemia.
    • Chronic infection – no symptoms
    • Acute infection – gastritis with pain, dyspepsia
    • Incidence in third world countries up to 80%.In USA around 30% after the age of 30.
    • Two types of H pylori gastritis – Antral predominant and corpus predominant.
    • Antral predominant patients get better after Hp treatment
    • GERD gets worse in pt with corpus predominant gastritis treatment
    • Corpus gastritis associated with Gastric Ca. It is more common in the Far East.
    • Diagnosis can be made by
      • Fecal antigen
      • Serum testing(but once positive, will always be positive even after successful treatment)
      • Endoscopic bx (and either by histology or by clo test which checks for the ability of the bacteria to lyse acid and produce ammonia)
      • Breath test.
    • < >< >Suppress acid for 4 – 8 weeks
    • Requires a combination of 2 antibiotics for at least 7-14 days.
    • Antibiotics used include biaxin, amoxicillin(prevpac), flagyl (high incidence of resistence), doxycycline, Levaquin, Nitaxonide (Alinia), peptobismol.
    • Treatment could be triple therapy, quadruple therapy, sequential therapy and LOAD.
    • Treatment efficacy is between 70-90%.
    • High incidence of resistance to Flagyl and Levaquin.
    • Sachromycis boulardi – less side effects to Rx.Lactobacillus gastrii use before treatment for 3 weeks
  • Hp Pearls:
    • DU patients have a lower incidence of gastric cancer, even though HP positive
    • Cag A positive strain is associated with higher chance of gastric cancer
    • Environmental factors for gastric cancers are, high salt intake, low fruits and veg. intakes, high nitrate diet.
    • AGA guidelines for dyspepsia
    • Check for HP if neg response to PPI
    • Stool antigen and urea breath test NOT recommended anymore
    • Some benefit of treating Hp in dyspepsia
    • All regimens are 70-90% successful
    • Lansoprazole amoxicillin, clarithromycin
    • LOAD – levo, omeprazole, Alinia and doxycycline
    • Patients with history of family hx of gastric cancer, should be screened for Hp
    • 60% of gastric cancer pt have Hp
    • Check for Hp in patients with ITP, atrophic gastritis and unexplained iron def
    • Always check for in pts with PUD, MALT, unexplained bloating, long term NSAID use, and family history of gastric cancer
    • False neg in pt with bleeding or long term PPI use
  • < >< >< >Pernicious anemia related
  • Crohns disease
  • Type A- autoimmune, achlorhydria, fundus, pernicious anemia
  • Type B– Bacterial. H pylori and in Antrum.
  • Peptic ulcer disease- Denudation of mucosa extending into muscularis propria layer due to gastric acid exposure
    • Causes include H pylori, NSAID, malignancy, crohns disease, syphilis, amyloid, herpes infections
    • 3 other ulcers have special names
      • Cushing ulcers (ulcers in stomach from stress eg. Vent. Pts)
      • Curling ulcers (ulcers in stomach in burns patients)
      • Cameron erosions (ulcers in hiatal hernia sac, often missed and cause of GI bleed of unknown origin)
    • 15% of gastric ulcers are painless – remember NSAIDs are given to relieve pain!
    • If there is no obvious cause of a GU, it probably is an H pylori infection
    • H pylori infection migrates from antrum to body of stomach when pt is on PPI
    • Repeat EGD to document healing!
    • Complications include bleeding, perforation, stricture and obstruction
    • If multiple ulcers suspect NSAID or rule out gastrinoma (Zollinger Ellison syndrome).Check fasting gastrin level and pH of acid in stomach.
    • NSAIDs can cause multiple ulcers in small bowel also
    • Pain of PUD is not typical.Classic teaching is GU pain is immediately after meals and DU pain gets better with meals but comes back with vengenance 2 hours later.
    • Always look for other causes including biliary, gall bladder, cardiac, IBD, pancreatic, ovarian
  • Gastric Bleeds:
    • < >Hemetemesis – fresh red color vomiting or coffee ground.
    • Coffee ground emesis. Older blood that has changed color.
    • Gastro occult vomiting.Means vomiting that tested positive for occult blood.
    • Melena – black tarry stools.Usually means upper GI bleed occasionally lower.
    • Hematochezia – Red color rectal bleeding
    • Heme occult – Normal color stool that is guiaic positive
      • Occult bleeding.Bleeding that is not obvious but still leads to iron def. anemia.
  • < >Hemetemesis and coffee ground emesis means bleeding from either stomach, esophagus or duodenum.Common causes include GU, DU, gastric erosions, esophageal ulcers, Mallory Weis tear, AVMs, portal gastropathy, GAVE, Dieulafoys, esophageal or gastric varices.
  • Varices usually present as fresh red color vomiting.
  • Gastro occult positive does not help at all.
  • Upper GI bleed if brisk can present as hematochezia.
  • Absence of bile in NGT aspirate does not rule out a DU.
  • Presence of bile and an otherwise clear NGT aspirate makes an UGI bleed less likely but does not rule it out.If in doubt do an EGD.It takes 5 min!
  • How to evaluate a GI bleed
    • Vitals, Vitals, Vitals!
    • Start 2 18 gauge IV access on 2 separate upper extremities!
    • Check CBC, PT, Liver panel (as bare minimum).
    • Stabilize patient before EGD.
    • If UGI bleed, NGT with lavage
  • Lavage – cold water lavage causes hemolysis.No added advantage.
  • You can facilitate lavage by giving IV erythromycin or reglan
  • If active bleeding start a PPI drip after a bolus.
  • If variceal bleeding suspected start octreotide 50 mcg in 30 min bolus followed by 50 mcg/hour drip
  • High BUN suggests an UGI bleed.It can also suggest volume depletion
  • Correct coagulopathy. Eg. If PT INR is greater than 2, correct with FFP.If platelet is less than 50,000 and patient is actively bleeding, give platelets.
  • When do you transfuse?No hard and fast rule.Depends on how fast Hb drops and comorbid conditions.
  • Mallory Weiss tear can occur from the first episode of vomiting!It is a tear that can occur either on gastric (usually 2/3 of cases) or esophageal side of GE junction.
  • 1/3 patients with known variceal bleeds in past can bleed from other reasons!
  • < >Rx of varices
    • Stabilize and banding. Obliterate varix by repeating EGD every 2 weeks.
    • IV octreotide
    • Switch to nadolol, coreg or inderal when stable
    • If banding fails, TIPS (trans jugular intrahepatic porto systemic shunt).Aim is to reduce pressure to less than 12.
    • If all fails, blackmore tube
  • Gastric varices – Use of “glue”.Risk is embolization and stroke
  • After healing of gastric varices patients can develop esophageal varices.
  • Lower GI Bleeds
    • Hematochezia – causes usually diverticular bleed or AVM.If chronic, think of IBD, SRUS, radiation proctitis etc.In some rare instances it can be an UGI source.If very bright red and no clots could be hemorrhoid
    • Heme occult positive.Look for polyps more than 1 cm, colon cancer, false positive or AVM.Diverticular disease does NOT cause heme occult positive.
    • < >Occult GI bleed (iron def, no obvious source, usually is an AVM often hiding in small bowel.May need capsule endoscopy for evaluation).
    • Dark stools can occur with iron, peptobismol also.
  • Gastric Cancer
    • Top 3 cancers in the world are lung, breast and colorectal cancer
    • Top 3 causes of death from cancer in the world is lung, gastric cancer and liver cancer.Gastric cancer is around 10%
    • Risk factors
      • H pylori
      • < >Role of refrigeration
      • Migration / environmental factors
      • Salt / nitroso compounds, gastric surgery, intestinal metaplasia, dysplasia, EBV virus?
    • Screening only in endemic areas eg. China, Japan
    • H pylori eradication
    • Signs and symptoms include
      • Dysphagia, pseudoachalasia, early satiety, weight loss, epigastric pain, mass felt on palpation etc
      • Virchow, Krukenberg and Sister Mary Joseph nodule
    • Diagnosis is with EGD.Adjuvant diagnostic testing always includes CT.It may also include PET scan, EUS, staging laproscopy, chest xray,
    • Early gastric cancer
      • When the cancer is limited to the mucosa and sub mucosa regardless of the presence of nodes.
      • Can be treated endoscopically.
      • The best success rate is from the Japanese literature.
    • Liver Disorders
    • Liver Anatomy:
      • Zone 1 – periportal zone
      • Zone 2 – intermediate zone
      • Zone 3 – Pericentral zone (contains P450 cytochrome, alcohol hepatitis, ischemia)
    • < >Nerve, Artery, Vein, Empty space, Lymphatics
    • Diaphragmatic hernia
    • Direct and Indirect Inguinal hernias
    • Femoral hernia
  • Bilirubin Cycle
    • Bilirubin Cycle
    • Heme to unconjugated bilirubin to Unconjugated bilirubin albumin complex to UDP glucoronosyl transferase to conjugated bilirubin.
  • < >< >Viral infections such as Hepatitis A, B, C, EBV, CMV, yellow fever virus, mumps,
  • Bacterial infections like legionella, leptospira
  • Genetic diseases like hereditary hemochromatosis, Alpha one antitrypsin deficiency, Wilsons disease
  • Autoimmune diseases like Primary biliary cirrhosis (PBC), autoimmune hepatitis (AIH),
  • Medications like INH, rifampin, cipro, tylenol, NSAIDs
  • Toxins like alcohol, aflatoxin
  • Biliary obstruction
  • Miscellaneous causes like CHF, Budd chiari syndrome
  • 3 different kinds of pictures
    • Predominantly hepatitis like.Mostly an elevation in ALT and AST
    • Predominantly cholestatic.Mostly an elevation in alkaline phosphatase
    • < >Use ALT /Alk Phos ratio.More than 5, less than 2 and in between is mixed.
  • < >First check the pattern.Is it predominatly cholestatic?If it is cholestatic then the possible causes are
    • PBC, chronic biliary obstruction, some cases of alcoholic hepatitis (less than 10% of cases)
  • So, if it is not cholestatic, then you have to look for the rest of the other causes.That means you have to do the following tests (in the least)
  • Hepatitis panel
  • AMA, ASMA, Alpha one antitrypsin phenotype, iron studies, anti LKM antibody, ceruloplasmin level, urinary copper excretion, ANA
  • US and or CT of liver
  • < >Get the history.Especially check medications, NSAID use, OTC tylenol use and herbal medications.Check when the LFT was last normal
  • Look for CHF.Biopsy shows nutmeg pattern.
  • < >If the patient has a high alkaline phosphatase it could be from 3 sources
    • < >< >< >So, if it is elevated from liver, the GGT or 5’ nucleotidase would be elevated.
    • Otherwise look for the elevation from the bone or pregnancy.
  • Get history
  • Typical pattern of alcoholic hepatitis is AST : ALT ratio is more than 2Ratio of 3 and above is diagnostic of alcoholic hepatitis
  • 10% of alcoholic hepatitis may present as cholestatic liver disease
  • Patients with alcoholism can have a high PT from malnutrition and a low platelet count from alcohol induced bone marrow depression.Makes it difficult to differentiate from cirrhosis
  • Alcoholic Hepatitis
    • If the patient has severe alcoholic hepatitis, the may need prednisone.You can assess severity by a formula called “discriminate function”.The formula uses the patients bilirubin and PT/INR
    • No other specific treatment works.Pentoxifylline and NAC have been tried.
    • 50% of patients with alcoholic hepatitis already have cirrhosis
    • 50% of them will progress to cirrhosis
    • If DF > 32, 30 day mortality is 30%!
    • If MELD score is more than 21 – 20% mortality in 90 days
    • Lille Score and Glasgow scores.www.lillemodel.com
    • Enteral treatment and NAC if Lille score is more than 0.45
    • Approach for Alcoholic hepatitis is as follows
      • Rule out infection by Xray, blood cultures, U/a, peritoneal tap
      • If neg, start 40 mg prednisone and NAC.
      • Reassess at 7 days with Lille score.If lille is more than .45 at 7 days 27% survival otherwise 77% survival
  • < >Alcoholism in USA is 8.5%
  • Risk of cirrhosis is 14% in men and 8% in women
  • 2.3 million years of work lost in 2001 alone due to alcohol related problems
  • Genetic predisposition
  • The single question “How many times in the past year have you had X or more drinks in a day?”, where X is 5 for men and 4 for women, is recommended for use by the National Institute on Alcohol Abuse and Alcoholism [20]. This is a modification of the third question of the AUDIT.
  • Have you ever felt the need to Cut down on drinking?
  • Have you ever felt Annoyed by criticism of your drinking?
  • Have you ever had Guilty feelings about your drinking?
  • Do you ever take a morning Eye opener (a drink first thing in the morning to steady your nerves or get rid of a hangover)?
  • Moderate drinking: low risk for alcohol problems
  •      – All women and men age ≥65: ≤1 drink per day
  •      – Men < age 65: ≤2 drinks per day
  • Heavy drinking: at risk for alcohol problems
  •      – Women: >7 drinks per week or 3 drinks per occasion
  •      – Men: >14 drinks per week or 4 drinks per occasion
  • Binge drinking:
  •      – Women: 4 or more drinks in a row
  •      – Men: 5 or more drinks in a row
  • < >Tylenol causes 50% of liver injury in USA
  • 15% transplants are from DILI
  • Upto 3 %hospitalization is from DILI
  • Second most common cause after tylenol is antibiotics.Amoxicillin-clavulanate is 60%.Others are NSAIDs, paroxetine, NFT, INH, CNS drugs, immunomodulatory drugs.
  • Two types – Hypersensitivity and Metabolic idiosyncrasy.
  • Dabigatrin – liver toxicity
  • Ok to use statins even if patient has NAFLD, HCV etc.Risk of statin related injury is 1 in a million
  • Herbal medicines that cause injury are skullcap, ma huang, chaparral, gerrymander, comfrey, lipkinetix, kava, ephedra
  • HLA – B 5701 MUST be checked before prescribing abacavir.
  • Hepatitis C
    • Viral infection
    • Acquired usually through IVDA, snorting cocaine, tattoos,
    • Sexual transmission rate is low – around 3%
    • Maternal Fetal transmission is low around 3% unless mother is HIV positive
    • Usually asymptomatic.
    • Rare symptoms include cryoglobinemia (joint pain, skin lesions, renal failure), corneal ulcers (moorens ulcer), Porphyrea cutanea tarda,
    • Six different types.Response rate varies based on type of Hepatitis C.Commonest ones in USA are Type 1 (80%) and type 2. Less common is type 3.
    • Response rate in Caucasians depends on the RVR (rapid virological response).
    • RVR depends on ILB-28 host genetics Types are CC, TT or CT
    • Response rate in african american population and hispanics is low.Usually around 30-40%
    • Response rate is lower if the patient has long standing disease, more fibrosis, HIV, etc
    • All patients should be immunized against Hepatitis A and B
    • Treatment is Pegylated interferon with ribavarin.Add a protease for 3 months if Type 1.
    • Type 2 – treat for 6 months.
    • Type 1.Treat for 2-3 months.Harvoni once daily..Cure rate is around 95%.
    • You can assess cirrhosis or fibrosis by either getting a liver biopsy or getting a blood test called Fibrosure or fibrotest or Hepascore.
    • Always check for AFP and if patient has cirrhosis check US every 6 months.
    • After having the disease for 30 years patients can develop cirrhosis and another 10 years hepatoma or liver cancer
    • Cirrhosis is a contraindication to treatment
    • Review side effects of treatment in detail with patients.Side effects include hair loss, retinopathy, thyroid dysfunction, pulmonary fibrosis, weight loss, neutropenia, anemia, thrombocytopenia, flulike symptoms and teratogenecity.
  • Hepatitis B
    • Viral infection
    • 70% have a subclinical infection
    • 30% have a icteric infection
    • 0.5 % have fulminant hepatitis
    • 3 possible outcomes
      • < >< >Chronic Hepatitis B
    • Extrahepatic manifestations
      • Polyarteritis Nodosa
      • Glomerular disease including nephrotic syndrome
      • Serum sickness like illness
    • < >Acute phase.Supportive.Rare patients may benefit with antiviral treatment.Interferon is contraindicated
    • Chronic hepatitis B.Interferon vs. oral antiviral medications.Options include lamivudine, telbivudine, adefovir, entecavir.
    • Chronic hepatitis B patients and carriers must be monitored for hepatomas.The best protocol for monitoring is MRI every 6 months and AFP.
  • This can be prevented.
  • Universal vaccination !
  • Patients with chronic hepatitis B should get hepatitis A vaccination
  • Hepatitis A
    • Viral infection
    • Transmission is via fecal oral route or male homosexual activity
    • Mostly in underdeveloped countries
    • Less than 0.3% develop fulminant hepatitis.
    • Everyone with liver disease of some sort should be vaccinated against hepatitis A.
    • Usually patients resolve completely
  • < >About 30% of the US population will have fatty changes on the liver.
  • 80% of the patients with BMI greater than 35 will have steatosis
  • There is a more ominous subtype of NAFLD which is called NASH (non alcoholic steatohepatitis).These patients progress to cirrhosis
  • Most of these patients have insulin resistance.This is marked by the metabolic syndrome and patients have 3 or more of the following
    • Waist circumference > 102 cm for males and > 88 for females
    • TG > 150
    • HDL < 40 or 50
    • BS > 110
    • BP > 130/85
  • Usually asymptomatic.
  • A rare patient may have some RUQ discomfort, hepatomegaly or fatigue
  • < >Non alcoholic steatohepatitis.
    • The only way to differentiate from the benign NAFLD is by liver biopsy.Non invasive methods being investigated are MRIs, Fibrosure
    • Predictors of NASH are AST:ALT > 1, older age,DM, HTN, insulin resistance
    • This can progress to cirrhosis
    • < >Use Fibrosure.
  • Patients with cryptogenic cirrhosis probably had NASH.
  • Treatment is weight reduction
  • Glucophage maybe helpful in patients with insulin resistance
  • Hereditary Hemocromatosis
    • Iron overload from heriditary causes
    • The culprit is increased iron absorption
    • Suspect hemochromatosis in patients with iron saturation > 45%
    • If saturation is greater than 45%, check for hemochromatosis gene. Four types, Type 1 is classical
    • Type 2 is Juvenile – HJV and HAMP mutation
    • Type 3 in Japan with TFR2 mutation
    • Type 4 Ferroprotein recepter abnormality
    • LFT abnormality maybe minimal or may even be normal
    • They can develop hepatomas
    • Iron deposit in the skin leads to bronze discoloration, in the pancreas causes diabetes, cardiomyopathy by deposit in the heart, pitutary deposits lead to sexual dysfunction and arthritis (typical is 2 and 3 MCP)
    • Can set off metal detectors if more than 50 gm iron accumulated.
    • Bronze diabetes
    • Treatment is to bring iron saturation to <30% and ferritin to less than 50
    • Phlebotomy is the best option
    • The blood from phlebotomy can be used by blood bank.
    • Dietary counseling (red meat, vitamins, avoid vitamin C) and avoid sea food (Vibrio vulfinicus)
    • Future – Hepcidin assay!
  • Autoimmune Hepatitis
    • Two types.Type 1 and 2.
    • Type 1 is in adults and they have ASMA positive
    • Type 2 in children and they have anti LKM positive
    • Disease is fatal if not treated.50% die within 2 years.
    • Treatment is prednisone with or without imuran.
  • Primary Biliary Cirrhosis
    • Cholestatic picture
    • Treatment is urso
    • They have a variety of other autoimmune diseases
    • Higher incidence of osteoporosis, fat soluble vitamin deficiency
  • Wilson’s Disease
    • < >Associated with copper metabolism abnormality
    • Rare after 40
    • Non hepatic manifestations include neuropsychiatric disturbance, hemolysis (high LDH), KF ring in the eye, Fanconi syndrome in the kidneys
    • Copper is Hella BAD
      • Ceruloplasmin, cirrhosis, corneal deposis, copper accumulation and carcinoma
      • Hemolytic anemia
      • Basal ganglia degeneration
      • < >Dementia, dyskinesia dysarthria.
  • Hepatitis B Curve:
    • Anti HB s Ab means immune with vaccination
    • Anti HBc Ab means immune with infection in past if anti Hbs Ab positive also
    • Anti HB c Ab positive with neg Hb s Ag neg andAg neg could mean four things
      • False positive of HBc Ab, old cured infection, chronic infection with undetectable HbsAg or recovering from an acute infection.
  • Cirggler Najjar Syndrome – absent glucloronyltransferase. Die in the first 2 years of life.If type 2, can live longer, treat with phenobarbital.Lack enzyme to conjugate bilirubin
  • Dubin Johnson syndrome – impaired excretion of bilirubin after conjugation
  • Rotor is milder form of Dubin Johnson
  • Reye Syndrome
    • Fatal childhood disease
    • Microvesicular fatty liver disease with low BS, vomiting , enlarged liver and coma
    • Occurs with use of Aspirin
    • B oxidation is reduced by inhibition of mitochondrial enzymes.
    • Avoid ASA in children except in those who have Kawasaki disease
  • Hepatitis E
    • Viral infection that is more common in 3rd world countries
    • Seroprevelance in USA is 21% !!!! But is probably from a milder genotype 3 HEV exposure
    • Fatal in pregnant women
    • Does not chronic disease
    • In developed countries comes from eating liver, pig meat, dear meat, rodent, boar meat.
    • No Rx available.
  • Hepatic Tumors
    • Benign lesions
      • < >Increases in incidence with age
      • Usually US or CT is characteristic.
      • For lesions smaller than 1 cm, MRI is best
      • Usually asymptomatic unless very large
      • No treatment needed.
    • < >Commonest benign lesion after cysts
    • < >Extremely low risk of rupture, even if large.
    • No malignant potential
    • Diagnosis by CT scan with hemangioma protocol or MRI or technicium scan
  • Focal nodular hyperplasia
    • Benign condition
    • More common in women in their 30’s to 40’s
    • No association with oral contraceptives
    • No malignant transformation
    • Observation is sufficient
    • Characteristic CT appearance.
  • Hepatic adenoma
    • Occurs mostly in women more than 30 and premenopausal
    • Strong association with oral contraceptives
    • Can rupture esp. during pregnancy
    • Can present as RUQ pain
    • Extremely difficult to differentiate from HCC.
    • May need resection.
    • Malignant transformation can occur.
  • Nodular regenerative hyperplasia
  • Inflammatory pseudotumor
  • Amebic liver abscess
  • Pyogenic abscess
    • Liver abscess occurs from either hematogenous spread or directly from adjacent areas.
    • Patients have multitude of non specific symptoms like fever, chills, abd. Discomfort
    • History and CT scan would be diagnostic.They often need surgery / drainage.
  • < >Hepatocellular carcinoma (HCC or hepatoma)
    • Malignant tumor of the liver
    • Usually occurs in the setting of chronic liver disease
    • Symptoms include weight loss, early satiety, upper abdominal pain, fever, SOB and paraneoplastic symptoms.
      • Paraneoplastic syndromes include
        • Hypoglycemia usually occurs from metabolic demands of the tumor.5% of the tumors secret insulin like growth factor and can cause severe hypoglycemia
        • Erythrocytosis can occur from erythropoietin secretion
        • Hypercalcemia occurs from bony metastasis or from secretion of parathyroid like protein.
        • Watery Diarrhea occurs from gastrin,VIP or prostaglandin-like immunoreactivity
    • Compensated liver disease becomes decompensated when patients develop HCC
    • Bony pain occurs with bony mets
    • Skin lesions are common but not pathognomonic.They include
      • < >< >Seborrheic keratosis
      • Pitryasis rotunda
      • < >Diagnosis is confirmed by an elevated AFP with a characteristic CT or MRI appearance.
      • Risk factors include Hepatitis B, Hepatitis C, Hemochromatosis, PBC and cirrhosis from alcohol.
      • Treatment is OLT.Chemotherapy, Radiofrequency ablation, Transarterial chemo embolization, radiation, percutaneous alcohol or acetic acid injection are other options.
    • Metastatic tumors
    • < >Rare tumors like sarcomas etc
  • Paraneoplastic syndromes include
    • Hypoglycemia usually occurs from metabolic demands of the tumor.5% of the tumors secret insulin like growth factor and can cause severe hypoglycemia
    • Erythrocytosis can occur from erythropoietin secretion
    • Hypercalcemia occurs from bony metastasis or from secretion of parathyroid like protein.
    • Watery Diarrhea occurs from gastrin,VIP or prostaglandin-like immunoreactivity
  • < >End stage liver disease where the normal tissue is replaced by fibrosis and forming nodules.
  • Two types – compensated or decompensated
  • It is called decompensated when they develop varices, ascites, encephalopathy or jaundice
  • < >Ascites and pedal edema
  • < >Spider angiomas
  • Caput medusae
  • Palmer erythema
  • Muscle wasting
  • < >Child-Pugh Turcotte
    • Modified Child-Pugh classification of the severity of liver disease according to the degree of ascites, the plasma concentrations of bilirubin and albumin, the prothrombin time, and the degree of encephalopathy. A total score of 5-6 is considered grade A (well-compensated disease); 7-9 is grade B (significant functional compromise); and 10-15 is grade C (decompensated disease). These grades correlate with one- and two-year patient survival: grade A – 100 and 85 percent; grade B – 80 and 60 percent; and grade C – 45 and 35 percent.
  • Variceal Bleed
    • Two types – gastric and esophageal
    • Acute gastric variceal bleed – Treatment is TIPS (transjugular intrahepatic portosystemic shunt)
    • Esophageal varies – Banding.
    • Medications can help prevent variceal bleed by 80%. Non selective beta blocker such as propranolol or nadolol or coreg should be used
    • Acutely Octreotide drip or terlipressin should be used.
    • Drawback of TIPS is that it can lead to hepatic encephalopathy
    • It does not change mortality
      • Hepatic Encephalopathy
        • Mental status change from the toxic effects of ammonia occuring in patients with liver disease
        • 3 types
        • Type A is when they have fulminant hepatic failure
        • Type B when encephalopathy occurs in the setting of TIPS
        • Type C occurs is when it occurs in the setting of cirrhosis.This type is rarely fatal
        • < >< >< >< >< >Ammonia levels are unreliable and correlate poorly with HE.
      • Features include asterexis, fetor hepaticus.
        • EEG findings are supportive.
        • Treatment is to remove precipitating causes
        • GI bleed, dehydration, infections, high oral protein diet, constipation, use of narcotics or sedatives.
      • Agents used to decrease ammonia in the gut
        • < >Rifaximin or xifaxan
        • Neomycin
        • < >Probiotics can help, Zinc can help but no definitive studies
        • Flumazenil and LOLA (L ornithine L aspartate)
      • Role of reporting and discussion with patient and family of work, driving and operating hazardous equipment
  • Hepatorenal Syndrome
    • Functional renal failure that occurs in patients with cirrhosis
    • Two types
      • Type I.Acute onset, high mortality with median survival 2 weeks
      • Type 2.Slower progression and better survival
    • Diagnosis of exclusion.
    • Urine sodium is less than10
    • < >Adequately hydrate patient, discontinue agents that can lead to renal failure, treat sepsis and GI bleed, etc
    • Mainstay of treatment is OLT.
    • Strategies to support the patient while waiting for OLT include
      • Octreotide with midodrine
      • < >Albumin infusions
      • Norepinephrine drips
      • < >Hepatopulmonary Syndrome
        • Patients become hypoxic from vasodilation occuring in the lungs from cirrhosis.
        • Treatment is OLT.
      • Portopulmonary HTN
        • < >Vasconstriction occurs in the pulmonary veins from the vasoconstrictive substances that bypass the liver.
        • OLT is contraindicated.
      • < > build up of fluid in abdominal cavity. Can be gradual or acute. Commonest cause is cirrhosis
      • Other causes include malignancies, cardiac causes, renal failure, TB, ovarian tumors, etc
      • Can present as isolated pleural effusion esp. right side from a diaphragmatic defect!(5% of the patients!)
      • Legs swell up first = heart
      • Belly swells frist – liver
      • Use a SAAG gradient,
      • 5% just show up with pleural efflusion, not always ascites
      • 2 important things to remember
        • < >PMN count more than 250 implies infection.
      • < >Salt restriction
      • Fluid restriction
      • Spirinolactone. Watch for K.Correct dose is 100 mg / day all at once and increase as needed.
      • Add lasix if hyperkalemia develops or inadequate response
      • < >10% of patients become unresponsive to diuretics.
      • If more than 5 liters removed, give 6-8 grams of albumin / liter. It usually comes in a 25gm bottle.(every 3 liters give one bottle).
      • TIPS is an alternative in some of these patients
    • Initial Tap
      • Initial tap
      • Send off cell count with diff, albumin, protein, gram stain, C and S (must be sent in a blood culture bottle), AFP, cytology, amylase,
  • Acute Liver Failure
    • Liver failure ocuring in the absence of cirrhosis but in less than 26 weeks.It is associated with liver injury, hepatic encephalopathy and high INR.
    • Three types hyperacute (less than 7 days), acute7 to 21 days, and subacute 3 weeks to 26 weeks.
    • Acute pts have cerebral edema and subacute of renal failure and portal HTN
    • < >No specific signs or symptoms except jaundice, abd. Pain, nausea, fatigue,vomiting etc.
    • Treatment done in a Univ. center where OLT is available
  • Bud Chiari Syndrome
    • Thrombosis of hepatic vein
    • Causes – look for hypercoagulable conditions
    • Testing is CT and US with dopplers of hepatic vein
    • Remember to differentiate it from portal vein thrombosis
  • Spontaneous Bacterial Peritonitis– occurs in the absence of an apparent intra-abdominal source of infection
    • Spontaneous bacterial peritonitis.High mortality if untreated promptly.
    • Unlike other peritonitis, this can be painless and patients may not have abdominal tenderness
    • Cirrhosis with a PMN > 250 = SBP
    • IV ceftriaxone or Unasyn or a quinolone plus flagyl
    • Avoid aminoglycosides
    • 70% recurrence rate after one episode.They must go home on prophylaxis with norfloxacin 400 mg daily.
    • Any patient getting variceal bleed must be given prophylactic antibiotics to prevent SBP
  • Pancreas Disorders
  • The Pancreas
    • Mixed endocrine and exocrine glands, consisting of lobar subunits composed of acini
    • Lies in retroperitoneal space of upper abdomen, which makes diagnosis very difficult
    • Pancreas resection also must accompany vessels, lymph nodes, duodenum, GB, spleen, upper jejunum, and part of stomach. This is a whipple procedure.
  • Embryology of the Pancreas:
    • Ventral bud and dorsal bud
    • Abnormality can cause pancreas divisum and annular pancreas
    • Remember 8 week mark!!!
  • Acute pancreatitis
    • Acute inflammation of the pancreas.
    • 80% of the cases are from alcohol and gallstones
    • Less common causes include
      • High TG, post ERCP, malignancy, medications, blunt trauma to abdomen, infections like ascariasis, mumps,coxsackievirus, pancreas divisum, vasculitis, cystic fibrosis, heriditary disease, hypercalcemia and AUTO IMMUNE Pancreatitis AIP
      • GET SMASHED (gallstone, ethanol, trauma, steroids, mumps, autoimmune, scorpion bite, hypercalcemia, high TG, ERCP, drugs.
    • < >< >FAST VET (furosemide, azathioprine, sulfa, thiazides, valproic acid, estrogent, tetracycline), most of the HIV drugs, INH, zantac, nitrofurantoin, Ace Inhibitors,tylenol
  • Autoimmune pancreatitis is characterized by a sausage shaped pancreas, elevated G4 levels and a response to steroids.
  • Mutations of CFTR can cause pancreatitis without cystic fibrosis
  • Chromosome 7 mutation can lead to a hereditary form of pancreatitis.
  • Abdominal pain radiating to the back
  • Nausea, vomiting
  • Fever, tachycardia, tachypnea and hypotension can occur.
  • Patients maybe jaundiced
  • Forget about the Cullens sign and Grey Turners sign.
  • Check CBC, CMP, calcium, amylase and lipase.
  • CT of abd and pelvis
  • US of abd.Especially look for sludge.
  • Assess Severity
    • Ransons criteria
    • Modified Glasgow criteria
    • < >Rise in BUN or HCT is prognostic of poor outcome
  • < >Aggressive fluid and electrolyte resuscitation
  • Use of antibiotics in severe cases.Cipro and Primaxin are the 2 antibiotics that have been shown to help in severe pancreatitis. However, it has fallen OUT of favor lately
  • Nutritional support – enteral or TPN is NO LONGER advocated.Early nutrition is suggested.
  • < >< >Cardiovascular shock
  • Hypocalcemia and hypomagnesemia
  • < >Pseudocyst formation
  • Hemosuccus pancreaticus
  • Chronic pancreatitis
    • A condition where there is chronic inflammation of the pancreas
    • Chronic excessive alcohol use
    • Tropical chronic pancreatitis
    • Cystic fibrosis
    • Hereditary disease 20 genes associated with bad outcome
    • Ampullary stenosis, pancreatic tumors, pseudocysts
    • < >Autoimmune pancreatitis
    • Idiopathic causes
    • < >Abdominal pain relieved with leaning forward, nausea, vomiting steatorrhea, diabetes, weight loss
    • Pancreatic calcification is diagnostic but it is only present in 33% of the cases.EUS and ERCP are other modalities available to make the diagnosis
    • Management is mostly focused around pain management.Options include viokase, nerve blocks, modified Puestow procedure.
    • Bacterial overgrowth, gastroparesis, SIBO, osteoporosis, diabetes occurs in CP.
    • Check fecal elastase -1 fasting TG, stool fecal fat, stool H pylori, Hb, Ca 19-9, B 12, folate, vitamin ADE, celiac, IgG4, ANA, serum trypsin level
  • < >19 million Americans may suffer from this disease, only 2.5 million diagnosed and only 140,000 receive treatment.
  • a primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by continuous or periodic impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial
  • It can cause cardiomyopathy, higher incidence of death from all cancers, dangerous arrythmias, dementia, hypertension, stroke, psychiatric illnesses.
  • This is in addition to liver and pancreatic disease
  • Multiple social problems arise from it including homicide.
  • CAGE questionaire ( cut down, anger, guilt and eye opener)
  • Single question – 5 drinks in men or 4 drinks in womenon one day in any given year!
  • < >Besides rehab, medications that have been used include
  • < >Naltrexone during rehab
  • Acamprosate (campral) for maintenance of abstinence
  • < >< >Cholesterol and or bilirubin
  • Cholesterol stones more common – Female, fat, fertile forty
  • Other causes are crohns, cystic fibrosis, rapid weight loss, estrogen therapy, increasing age, native american
  • Pigment stones in alcoholics, hemolysis, biliary infection
  • Charcots triad – jaundice, fever, Ruq pain
  • Porcelin GB – calcified GB found incidentally.  Rx cholecystectomy