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GI Board Review.ppt

VIEWS: 18 PAGES: 149

									GI Board Review
2006


             Louis Chaptini, MD
Esophagus
   GERD:
       Heartburn
       Regurgitation
       Retrosternal burning
   Atypical manifestations
       Chest pain
       Asthma
       Aspiration
       Chronic cough
       Hoarseness
       Chronic laryngitis
       Dental erosions
Esophagus
   53 y/o with 10 y hx of heartburn
    presents to your OP clinic. The next
    step in the evaluation:
       Endosocpy
       Nexium 40 mg qd
       CBC
       Order esophageal manometry
       24 hr pHmetry
Esophagus
   53 y/o with 10 y hx of heartburn
    presents to your OP clinic. The next
    step in the evaluation:
       Endoscopy
       Nexium 40 mg qd
       CBC
       Order esophageal manometry
       24 hr pHmetry
Esophagus

   Lifestyle modification
       Weight loss
       Stop smoking
       Elevate head of bed
       Allow enough time between dinner and
        sleeping
Esophagus
   H2Receptor blocker
   PPI
       Most rapid and complete symptom relief
       Faster mucosal healing
   Endoscopy
       Screen for Barrett’s in long standing symptoms
       If alarm symptoms
           Dysphagia

           Anemia/Bleeding

           Weight loss
Esophagus
   Antireflux surgery
       Should be only considered in patients with
        resolution of symptoms on medical trt
       Same efficacy as PPI
       Before surgery esophageal manometry is
        necessary
   pHmetry
       To confirm the diagnosis in non erosive GERD
       Evaluate patients not responding to therapy
       Evaluate extraesophageal manifestations of
        GERD
Esophagus

   What is the most common cause of
    non cardiac chest pain?
       Esophageal spasm
       Nutcracker esophagus
       Achalasia
       GERD
       Biliary disease
Esophagus

   GERD is the most common cause of
    non cardiac chest pain
   The diagnosis is confirmed by 24h
    pHmetry or successful trial of PPI
    (usually high dose and for long
    term)
Esophagus

   The patient in the first case had an
    EGD with biopsy of an irregular GE
    junction that showed intestinal
    metaplasia/goblet cells.
       What is your diagnosis?
       What is the associated risk?
       How do you treat/manage this patient?
Esophagus
   Barrett’s occurs in patients with early age
    at onset and long standing heartburn
   Adenocarcinoma is now as frequent as
    squamous cell carcinoma
   Barrett’s is present in up to 10% of
    patients with GERD
   Screening for Barrett’s is appropriate in
       Older patients (>50)
       Long-standing GERD symptoms (>5 years,
        MKSAP 13 >1 year)
       Especially white men
Esophagus

   Periodic mucosal biopsy to look for
    dysplasia
   Esophagectomy should be
    considered with high grade
    dysplasia
   Smoking and drinking are risk
    factors for squamous cell cancer
Esophagus
Esophagus

   Dysphagia:
       Weight loss: think Cancer
       Intermittent: web, ring
       Solid and liquid: neuromuscular, diffuse
        esophageal spasm, scleroderma,
        achalasia
       Chronic GERD: peptic stricture
Esophagus
   Achalasia                         Nutcracker Esophagus
       Lack of peristalsis                High amplitude
       Incomplete relaxation               peristaltic contractions
        of LES
       Dg on esophageal              Hypertensive LES
        manometry
                                           High LES pressure
       Pneumatic dilation or
        surgical myotomy                   Normal LES relaxation


   Diffuse Esoph Spasms              Ineffective motility
       Simultaneous                       With scleroderma
        contractions with                  Weak peristalsis
        intermittent normal                Low LES
        peristalsis
       Nitrate, calcium channel
        blocker
Esophagus

   33 y/o men with HIV, unknown CD4
    count, presents for odynophagia for
    the past couple of days. He was
    taking doxycycline for one week.
       What is your differential diagnosis?
       How do you confirm it?
Esophagus
Esophagus

   Pill esophagitis: always on the
    board
   HIV patient with odynophagia:
       Candida
       HSV
       CMV
       Idopathic ulcer
   Severe esophagitis secondary to
    GERD can cause odynophagia
PUD

   What are the 2 most common
    causes of PUD?
       NSAID
       H.Pylori
       Steroids
       Idiopathic
PUD

   H.Pylori is responsible of
       50 to 80% of duodenal ulcers
       40 to 60% of gastric ulcers
       80% of gastric cancers
       90% of gastric lymphomas
   The lifelong incidence of ulcer
    disease in those infected with
    H.Pylori is only 20%
PUD

   You find an ulcer in the antrum of a
    43y/o female who presented for
    dyspepsia. What’s the next step?
       Biopsy
       Check H.Pylori serology
       Start PPI
PUD

   You find an ulcer in the antrum of a
    43y/o female who presented for
    dyspepsia. What’s the next step?
       Biopsy
       Check H.Pylori serology
       Start PPI
PUD
   Gastric ulcers should be biopsied to R/O
    malignancy, as opposed to duodenal
    ulcers.
   H.Pylori should be checked, usually on
    biopsy, if not possible serology is
    appropriate
   Detection of H.Pylori
       Endoscopic          o Non Endoscopic
          Culture             o   Antibody tests
          Histology           o   Urea breath test
          Urease testing      o   Fecal antigen test
PUD

   Treatment regimens
       PPI/Amox/Clarithromycin
       PPI/Flagyl/Clarithromycin
       PPI/Peptobismol/Flagyl/Tetracycline
   14 days better than 10 days
PUD

   Risk factors for NSAID induced GI
    complications
       Advanced age (>75)
       Pre-existing ulcer disease
       Multiple NSAIDs or high dose NSAIDs
       Concomitant steroid therapy or
        anticoagulant therapy
       Comorbid diseases
PUD

   Eradicating H.Pylori in NSAID users
    is still controversial
   But if NSAID induced gastropathy
    with H.Pylori, eradication is
    indicated
   NSAID gastropathy is a dose related
    phenomenon
   COX-2 selective NSAID result in
    fewer GI ulcers
Dyspepsia

   Endoscopy is indicated if
       Age greater than 50
       Alarm symptoms (weight loss, anemia)
       Patient concerned about serious
        disease
   Otherwise, test for H.Pylori
       If (+), treat
       If (-) , trial of H2Blocker or PPI
Case

   65 y/o presents with N/V, found to
    have thickened gastric folds.
    Differential includes:
       Zollinger Ellison
       MALT
       H.Pylori infection
       Menetrier’s disease
       All of the above
Case

   65 y/o presents with N/V, found to
    have thickened gastric folds.
    Differential includes:
       Zollinger Ellison
       MALT
       H.Pylori infection
       Menetrier’s disease
       All of the above
Case

   Biopsy was consistent with MALT
    lymphoma
       Treat H.Pylori if present
       Send for gastrectomy
       Chemotherapy
       Observation since it’s a benign
        condition
Case

   Biopsy was consistent with MALT
    lymphoma
       Treat H.Pylori if present
       Send for gastrectomy
       Chemotherapy
       Observation since it’s a benign
        condition
MALT/ZE

   70 to 80% of MALT will regress
    when H.Pylori is eradicated
   Think about ZE when
       Recurrent ulcers on treatment
       Chronic diarrhea
       Other endocrine disorders (MEN)
Case

   46 y/o with type I diabetes presents
    for N/V, early satiety, vague
    epigastric pain for the past 4
    months. His condition will improve
    with
       PPI
       Low fat diet, small meals, control of
        DM, and Reglan
       Eradication of H.Pylori if present
Case

   46 y/o with type I diabetes presents
    for N/V, early satiety, vague
    epigastric pain for the past 4
    months. His condition will improve
    with
       PPI
       Low fat diet, small meals, control of
        DM, and Reglan
       Eradication of H.Pylori if present
Gastroparesis
   Causes
       Drugs
       Systemic disease (DM, Scleroderma..)
       Idiopathic, post viral
   Diagnosis
       Gastric Emptying Scan
   Treatment
       Prokinetics
       Surgery
       Nutritional support
Case

   37 y/o female with epigastric pain is
    found to have lipase level of 1050.
    Her management includes the
    following except:
       IV fluids
       Pain meds
       RUQ US
       ERCP
       NPO
Case

   37 y/o female with epigastric pain is
    found to have lipase level of 1050.
    Her management includes the
    following except:
       IV fluids
       Pain meds
       RUQ US
       ERCP
       NPO
Acute Pancreatitis

   The most common cause is
       Gallstones
       P. Divisum
       Alcohol
       Medication
       Trauma
       Hypercalcemia
       High triglycerides
Acute pancreatitis
   True or False:
       Idiopathic pancreatitis: 10% of cases
       Cholecystectomy is indicated after the
        second bout of IP pancreatitis
       The management of necrotizing
        pancreatitis should be in ICU setting,
        may include CT guided aspiration and
        Abx therapy and sometimes surgical
        debridement
       Ranson’s score is calculated at
        presentation and is the best prognostic
        factor
        Acute pancreatitis
           True or False:
FALSE          Idiopathic pancreatitis: 10% of cases
TRUE           Cholecystectomy is indicated after the
                second bout of IP pancreatitis
TRUE           The management of necrotizing
                pancreatitis should be in ICU setting,
                may include CT guided aspiration and
                Abx therapy and sometimes surgical
                debridement
FALSE          Ranson’s score is calculated at
                presentation and is the best prognostic
                factor
Case

   55 y/o male with a history of
    chronic alcohol abuse presents with
    early satiety, nausea and vomiting.
    On exam he has a non tentder
    epigastric mass. The most likely dg:
       Pancreatic abscess
       Pseudocyst
       Gastric cancer
       Pancreatic cancer
Case

   55 y/o male with a history of
    chronic alcohol abuse presents with
    early satiety, nausea and vomiting.
    On exam he has a non tentder
    epigastric mass. The most likely dg:
       Pancreatic abscess
       Pseudocyst
       Gastric cancer
       Pancreatic cancer
Chronic pancreatitis

   True or False:
       Gallstones are the most common cause
        of chronic pancreatitis
       The characteristics of chr panc are
        pain, steatorrhea, diabetes and
        pancreatic calcification
       The presence of a pseudocyst is an
        indication for drainage to prevent
        infection
       Endoscopic drainage is only indicated if
        the panc duct is dilated
Chronic pancreatitis

   True or False:
       Gallstones are the most common cause
        of chronic pancreatitis FALSE
       The characteristics of chr panc are
        pain, steatorrhea, diabetes and
        pancreatic calcification TRUE
       The presence of a pseudocyst is an
        indication for drainage to prevent
        infection FALSE
       Endoscopic drainage is only indicated if
        the panc duct is dilated TRUE
Chronic pancreatitis

   Complications of chr panc
       Infection
       Pseudocyst
       Hemorrhage
       Fistulas
   Pancreatic enzymes have little or no
    effect on pain but help with
    steatorrhea
Case

   67 y/o male presents with weight
    loss, fatigue, anorexia and painless
    jaundice. What is your diagnosis?
       Lymphoma
       Pancreatic adenocarcinoma
       Cystic neoplasm of the pancreas
       Biliary stricture
       choledocholithiasis
Pancreatic adenocarcinoma

   The management of pancreatic
    cancer includes
       Tissue diagnosis
       Surgery if
          No metastsases
          No local invasion

          No vascular encasement

       Whipple procedure
        (pancreaticoduodenectomy)
       Palliative treatment
Diarrhea

   32 y/o female presents with 2 day
    hx of crampy abdominal pain and
    bloody diarrhea
       What is your differential?
       What if she is 75 y/o and has CAD and
        PVD?
       How do you manage this patient?
        Would you start abx?
Diarrhea

   The most common causes of acute
    bloody diarrhea
       Infectious dysentery
       IBD
       Ischemic colitis
Diarrhea
   Common causes of infectious dysentery
       Campylobacter, Salmonella
       Shigella, E.Coli
       Yersinia, Entameba, Aeromonas, Plesiomonas
   Seafood induced dysentery
       Vibrio parahemolyticus (mainly watery but can
        be bloody)
       Plesiomonas shigelloides
       Campylobacter
Diarrhea
   Parasites that cause bloody diarrhea
       Entamoeba Histolytica
       Balantidium Coli
       Dientamoeba fragilis
       Schistosomas
   Parasites that non-bloody diarrhea
       Giardia
       Cryptosporidiosis
       Cyclospora
Diarrhea

   45 y/o male with HIV presents with
    bloody diarrhea. The differential
    includes all of the following except:
       Gono, chlamydia, syphilis, Herpes
       CMV
       TB, Histoplasmosis
       Cyclospora
Diarrhea

   45 y/o male with HIV presents with
    bloody diarrhea. The differential
    includes all of the following except:
       Gono, chlamydia, syphilis, Herpes
       CMV
       TB, Histoplasmosis
       Cyclospora
Diarrhea

   HIV with non bloody diarrhea
       Cryptosporidium
       Isospora Belli
       Cyclospora
       Microsporidia
       Giardia
       MAI
Diarrhea

   4 hours after eating in a restaurant,
    a healthy men presents to the ER
    with several episodes of watery
    diarrhea. All of the following are
    possible except:
       Bacillus cereus
       Staph aureus
       E.coli
Diarrhea

   4 hours after eating in a restaurant,
    a healthy men presents to the ER
    with several episodes of watery
    diarrhea. All of the following are
    possible except:
       Bacillus cereus
       Staph aureus
       E.coli
Diarrhea
   True or False
       Rotavirus, Calciviruses (Norwalk),
        Adenovirus are all causes of acute
        diarrhea
       E.coli O157:H7 should be treated with
        quinolones
       Entertotoxigenic E.Coli is associated
        with HUS in 10% of the cases
       Yersinia Enterolytica can mimic
        appendicitis
       C.diff recurs in 20% of cases after
        successful treatment
Diarrhea
   True or False
       Rotavirus, Calciviruses (Norwalk),
        Adenovirus are all causes of acute
        diarrhea TRUE
       E.coli O157:H7 should be treated with
        Quinolones FALSE
       Entertotoxigenic E.Coli is associated
        with HUS in 10% of the cases FALSE
       Yersinia Enterolytica can mimic
        appendicitis TRUE
       C.diff recurs in 20% of cases after
        successful treatment TRUE
Diarrhea

   45 y/o obese female presents for
    chronic diarrhea for the past 4
    months. Stool studies and
    colonoscopy were normal. Stool Na
    30, K 40.
       What is the fecal osmotic gap in her?
       Would a stool pH be helpful in this
        case?
       What is your differential?
Diarrhea

   Fecal osmotic gap:
      280 – 2 x (Na+K)
    If >50 osmotic diarrhea
    If<50 secretory diarrhea
   With laxative abuse, the stools are
    acid (low pH), they will turn red
    with alkalinization
Diarrhea

   Causes of osmotic diarrhea
    (gap>50)
       Lactose intolerance
       Laxative abuse
       Intestinal malabsorption (celiac
        disease)
   With fasting  less than 500g of
    stools
Diarrhea

   Causes of secretory diarrhea
    (gap<50)
       Enterotoxin mediated infectious
        diarrhea
       Hormone mediated (gastrin, VIP,
        serotonin, calcitonin)
       Secreting villous adenoma
       Microscopic colitis
   With fasting  more than 500g of
    stools
Diarrhea

   Inflammatory diarrhea
       Neutrophils in the stools, colonic
        ulcerations
       Causes
          IBD
          Radiation colitis

          Enteroinvasive infections
Diarrhea

   Large volume
       Think about a proximal origin (small
        bowel..)
   Small volume
       Distal source (colonic..)
   Always look at the medications
   Endocrine causes: DM,
    Hyperthyroidism
   C.diff and Giardia can give chronic
    diarrhea
Diarrhea

   42 y/o male with iron deficiency
    anemia and chronic diarrhea. GI
    work-up including EGD,
    colonoscopy, capsule endoscopy is
    negative.
       What’s your diagnosis?
       What’s the next step?
       What’s the gold standard for the
        diagnosis?
       What is the skin manifestation
        associated with this condition?
Diarrhea
   Celiac sprue is caused by sensitivity to gluten and is
    characterized by malabsorption and diarrhea
   Antibodies to Gliadin, Endomysium and tissue
    transglutaminase are used for the diagnosis
   Small bowel biopsy is the gold standard for the
    diagnosis
   Complications include lymphoma, ulcerative
    jejunoileitis
   Dermatitis herpetiformis is the associated skin
    condition
   Tropical sprue is infectious in source and is identical
    to celiac sprue, Klebsiella and E.coli are
    incriminated.
Diarrhea

   45 y/o male lost 150 cm of ileum
    after an MVA and extensive
    abdominal surgery. He presents
    with diarrhea. TRUE or FALSE
       Cholestyramine will help and should be
        tried
       Antidiarrheal agents should be used
       Cholestyramine will worsen the
        diarrhea
Diarrhea

   45 y/o male lost 150 cm of ileum
    after an MVA and extensive
    abdominal surgery. He presents
    with diarrhea. TRUE or FALSE
       Cholestyramine will help and should be
        tried False
       Antidiarrheal agents should be used
        True
       Cholestyramine will worsen the
        diarrhea True
Diarrhea

   This is a guaranteed question
       If resection is < 100 cm,
        cholestyramine helps because the
        diarrhea is caused by colonic irritation
        by bile salts (bile salt diarrhea)
       If resection is > 100 cm, the bile salt
        pool is depleted and cholestyramine
        will NOT help.
       Memorize:
            RESECTION<100cmCHOLESTYRAMI
             NE
IBD
   Can simulate appendicitis

   Skip areas on endoscopy

   Smoking is protective in
                                Crohn’s disease
   Granulomas found on bx

   Crypt abscesses
                                UC
   Enterocutaneous fistulas

   75% positive for p-ANCA
IBD
   Can simulate appendicitis

   Skip areas on endoscopy

   Smoking is protective in
                                Crohn’s disease
   Granulomas found on bx

   Crypt abscesses
                                UC
   Enterocutaneous fistulas

   75% positive for p-ANCA
IBD
   Transmural inflammation

   Abdominal mass

    Backwash ileitis

                              Crohn’s disease
   Perianal disease
                              UC
   Crypt abscesses

   Malnutrition

   Rectal bleeding
IBD
   Transmural inflammation

   Abdominal mass

    Backwash ileitis

                              Crohn’s disease
   Perianal disease
                              UC
   Crypt abscesses

   Malnutrition

   Rectal bleeding
IBD

   Extraintestinal manifestations of
    Crohn’s
       Polyarticular arthritis
       E.Nodosum
       Pyoderma Gangrenosum
       Uveitits
       Nephrolithiasis
IBD

   35 y/o male with entercutaneous
    fistulas from Crohn’s disease should
    be treated with
       Surgery
       Infliximab
       Azathioprine
       Cyclosporine
IBD

   35 y/o male with entercutaneous
    fistulas from Crohn’s disease should
    be treated with
       Surgery
       Infliximab
       Azathioprine
       Cyclosporine
IBD

   What kind of kidney stones are
    associated with Crohn’s?
       Oxalate
       Cystine stones
       Uric acid
   Why?
IBD

   34 y/o female with history of UC
    presents for abnormal LFT. The
    differential includes:
       Fatty liver
       Chronic hepatitis
       PSC
       Pericholangitis
       All of the above
IBD

   34 y/o female with history of UC
    presents for abnormal LFT. The
    differential includes:
       Fatty liver
       Chronic hepatitis
       PSC
       Pericholangitis
       All of the above
IBD

   Extraintestinal manifestations of UC
       Arthritis
       Ankylosing spondylitis
       PG
       E. Nodosum
       PSC
       Uveitis
IBD

   Ankylosing spondylitis does NOT
    follow colitis activity
   Polyarthritis, PG, E. Nodosum follow
    colitis activity
   Patients with extensive UC for at
    least 8 years should be screened for
    colorectal cancer every 1 to 3 years
IBD

   Steroids can be used to induce
    remission in IBD, 5-ASA to maintain
    remission
   6-MP, Azathioprine (precursor of 6-
    MP), Methotrexate, Cyclosporine are
    steroid sparing agents
   Infliximab is used for fistulizing
    disease
   Surgery for stricturing disease
Colon Cancer
   Screening should begin at age ____
   The lifetime risk of developing CRC is ___
    %
   Genetic syndromes associated with high
    risk CRC are _____
   ___ % of adenomatous polyps will
    progress to cancer
   5-year survival
       Localized: ___ %
       Regional lymph nodes: ___ %
       Distant mets: ___ %
Colon Cancer
   Screening should begin at age 50
   The lifetime risk of developing CRC is 6 %
   Genetic syndromes associated with high
    risk CRC are FAP and HNPCC
   5 % of adenomatous polyps will progress
    to cancer
   5-year survival
       Localized: 90 %
       Regional lymph nodes: 65 %
       Distant mets: 7 %
Colon Cancer
   Screening
       For general population: FOBT every
        year and sigmoidoscopy every 3 to 5
        years
       HNPCC risk: colonoscopy at age 25 or
        10 years younger than youngest
        affected relative, q 2 years until age 40
        and then q year
       FAP: sigmoidoscopy at age 12, every 1
        to 2 years
       If adenoma > 1cm, or multiple
        adenomas: colonoscopy in 3 years
Colon Cancer

   Treatment:
       No nodes or mets: surgery
       Nodes: surgery + 5 FU
       Distant mets: surgery + 5 FU +
        resection of solitary met (lung, liver)
      Hepatitis
   50 y/o F obese, DM, ALT            Alcoholic Hepatitis
    112, AST 107
   35 y/o, drugs, alcohol, ALT        Hemochromatosis
    77, AST 89
   22 y/o, neuropsych sympt.,         Auto-immune hepatitis
    AST 165, ALT 40
   34 y/o, DM, arthralgia, skin       Wilson’s disease
    pigm., AST 100, ALT 122
   28 y/o F, rash, arthritis,         NASH
    increased globulins, AST
    97, ALT 80                         Hepatitis C
   44 y/o, alcoholic, T Bil 5, D
    Bil 3.3, Ast 180, ALT 100
        Hepatitis
   50 y/o F obese, DM, ALT            Alcoholic Hepatitis
    112, AST 107
   35 y/o, drugs, alcohol, ALT        Hemochromatosis
    77, AST 89
   22 y/o, neuropsych sympt.,         Auto-immune hepatitis
    AST 165, ALT 40
   34 y/o, DM, arthralgia, skin       Wilson’s disease
    pigm., AST 100, ALT 122
   28 y/o F, rash, arthritis,         NASH
    increased globulins, AST
    97, ALT 80                         Hepatitis C
   44 y/o, alcoholic, T Bil 5, D
    Bil 3.3, AST 180, ALT 100
Abnormal LFT
   Alcoholic Hepatitis      Discontinuation,
                              observation
   Hemochromatosis
                             ANA, ASMA, Anti LKM
   Auto-immune
    hepatitis
                             Ceruloplasmin, 24 hr
                              urine copper
   Wilson’s disease

   NASH                     Hep C Ab


   Hepatitis C              Ferritin, iron saturation

                             Response to weight loss
Abnormal LFT
   Alcoholic Hepatitis      Discontinuation,
                              obervation
   Hemochromatosis
                             ANA, ASMA, Anti LKM
   Auto-immune
    hepatitis
                             Ceruloplasmin, 24 hr
                              urine copper
   Wilson’s disease

   NASH                     Hep C Ab


   Hepatitis C              Ferritin, iron saturtion

                             Response to weight loss
NASH

   Risk factors:
       Obesity
       DM
       Hyperlipidemia
       Gastric bypass
       TPN
       Meds (amiodarone)
Alcoholic Hepatitis

   Role of steroids:
       DF: 4.6 x (PT – PT control) + T bil
       If > 32, steroids are indicated
Acute hepatitis

   19 y/o men, AST and ALT in the
    2000 range, jaundiced, PMH
    depression, recent travel to Cancun.
    Next step:
       Tylenol Level
       Urine drug screen
       Hepatitis serologies (acute panel)
       Steroids
       Empiric treatment with Mucomyst (17
        doses)
Acute hepatitis

   In the previous case, Ig M anti
    HAV+, PT 25, confused. Next step:
       Observation in ICU
       Liver transplantation evaluation
       Interferon/Ribavarin
       Interferon/Lamivudine
Acute hepatitis

   In the previous case, Ig M anti
    HAV+, PT 25, confused. Next step:
       Observation in ICU
       Liver transplantation evaluation
       Interferon/Ribavarin
       Interferon/Lamivudine
Acute hepatitis

   What about the household contacts?
       Hep A vaccine
       Hep A immunoglobulin
       Hep A vaccine + immunoglobulin
       LFT
       Wait and see
Acute hepatitis

   What about the household contacts?
       Hep A vaccine
       Hep A immunoglobulin
       Hep A vaccin + immunoglobulin
       LFT
       Wait and see
   Hep A vaccine should be given to
    travelers to endemic area: 0, 6m,
    12m (boosters)
Acute hepatitis

   33 y/o nurse presents after a
    needle stick with blood from patient
    with history of hepatitis B. the
    patient is HBS Ag (-) and Ab (+).
    The nurse should have
       Hep B immunoglobulins (HBIG)
       Hep B vaccine
       Check Hep B S Ab
       HBIG + vaccine
Acute hepatitis

   33 y/o nurse presents after a
    needle stick with blood from patient
    with history of hepatitis B. the
    patient is HBS Ag (-) and Ab (+).
    The nurse should have
       Hep B immunoglobulins (HBIG)
       Hep B vaccine
       Check Hep B S Ab
       HBIG + vaccine
Acute hepatitis

   What if the patient is Hep B S Ag
    (+) and the nurse is Ag (-) and Ab
    (-)?
       HBIG
       Hep B vaccine
       Both
       None
Acute hepatitis
   What if the patient is Hep B S Ag (+) and
    the nurse is Ag (-) and Ab (-)?
       HBIG
       Hep B vaccine
       Both
       None
   Other circumstances where HBIG should
    be administered
       Sexual exposure
       Parenteral exposure
       Vertical transmission
Hepatitis

   Chronic Hep B
       The risk of developing chronic hep B is
        inversely related to ___________
       The FDA approved trt for chr hep B is
        ___________
       In patients with chr hep B,
        hepatocellular carcinoma can occur
        w/o________
       _________is a sign of replication
Hepatitis

   Chronic Hep B
       The risk of developing chronic hep B is
        inversely related to age at acquisition
        of infection
       The FDA approved trt for chr hep B is
        Lamivudine and interferon and recently
        adefovir and entecavir
       In patients with chr hep B,
        hepatocellular carcinoma can occur w/o
        cirrhosis
       Hep Be Ag is a sign of replication
Hepatitis

   45 y/o, IVDA, presents for
    evaluation and treatment of Hep C
       Acute hep C progress to chronic in
        _____ of cases
       Progression from chronic hep C to
        cirrhosis occurs in ______ of cases
       HCC in cirrhotic develops in the range
        of _____ per year
Hepatitis

   45 y/o, IVDA, presents for
    evaluation and treatment of Hep C
       Acute hep C progress to chronic in 85
        % of cases
       Progression from chronic hep C to
        cirrhosis occurs in 5 to 20 % of cases
       HCC in cirrhotic develops in the range
        of 1-4 % per year
Hepatitis

   On exam, he has mild ascites,
    spider angiomas and splenomegaly.
    His ALT is 95, AST 93, T Bil 1.5, D
    Bil 0.9, AP 211, Plt 54. He’s asking
    about treatment for hep C
       He’s not a candidate because he has
        cirrhosis
       Because he has low platelets
       He can be treated with interferon only
       He can be started immediately on IFN
        and Ribavarin
Hepatitis

   On exam, he has mild ascites,
    spider angiomas and splenomegaly.
    His ALT is 95, AST 93, T Bil 1.5, D
    Bil 0.9, AP 211, Plt 54. He’s asking
    about treatment for hep C
       He’s not a candidate because he has
        cirrhosis
       Because he has low platelets
       He can be treated with interferon only
       He can be started immediately on IFN
        and Ribavarin
Hepatitis

   Contrindication for trt of hep C with
    IFN and Ribavarin
       Hb < 12, WBC < 1500, Plt < 100000
       Decompensated cirrhosis
       Poorly controlled DM
       Severe psychiatric illness
Hepatitis

   Extra intestinal manif of Hep C
       Hematologic (cryo, lymphoma)
       Autoimmune (thyroiditis, sjogren’s,
        ITP)
       Renal (GN, Membranous GN)
       Dermatologic (vasculitis, lichen planus,
        PCT)
       Rheumatologic (inflammatory arthritis)
Autoimmune Hepatitis

   Type I:
       Female
       ANA +, ASMA +,
        Hypergammaglobulinemia (IgG)
   Type II
       Anti LKM
       Childhood or early adolescence
   Type III
       No positive markers
Wilson’s disease

   Autosomal recessive
   < 35 y/o
   Hemolytic anemia, neuropathy,
    neuropsch symptoms
   Decreased ceruloplasmin level,
    increased urinary copper, increased
    hepatic copper content
   Kayser Fleisher rings
   Trt D-Penicillamine
Alpha 1 antitrypsin

   Normal phenotype MM
   Disease: ZZ
   Prevalence highest in white
    northern European
           PSC v/s PBC
   Men = Women

   Women > Men (9:1)

   Inc AP, AMA +

                                       PBC
   Associated with IBD
                                       PSC
                                       Both
   Urso decr rate of progression      None

   Urso can cure

   Liver transplant is curative

   Segmental intrahepatic and
    extrahepatic duct strictures
            PSC v/s PBC
   Men = Women

   Women > Men (9:1)

   Inc AP, AMA +                                     PBC

    Associated with IBD

                                                      PSC
   Urso decr rate of progression
                                                      Both
   Urso can cure
                                                      None
   Liver transplant is curative

   Segmental intrahepatic and extrahepatic duct
    strictures
Cirrhosis
   Beta blockers and endoscopic variceal
    ligation reduce risk of variceal bleeding
   Cirrhotic patients with evidence of clinical
    or biochemical decompensation should be
    considered for transplant
   SBP: PMN > 250, SAAG > 1.1
   TIPS is an option in refractory ascites but
    increase risk of encephalopathy
Cirrhosis

   Mean survival after onset of ascites
    or encephalopathy is 2 years
   Mean survival after SBP or
    refractory ascites is 6 months
   Screening for hepatoma is advised
    although efficacy is unknown
Liver transplant

   CI for LT
       Active HIV (?)
       Severe underlying medical illness
       Unresolved sepsis
       Active drug or alcohol abuse
       Unresolved extrahepatic malignancy
Liver and pregnancy

   32 y/o pregnant, 3rd trimester,
    referred for abnl LFT. AP 250, AST
    22, ALT 23, T bil 0.4. She’s
    asymptomatic. Differential includes
       Acute Fatty Liver of Pregnancy (AFLP)
       HELLP
       Pre-eclampsia
       Hepatitis
       None of the above
Liver and pregnancy

   32 y/o pregnant, 3rd trimester,
    referred for abnl LFT. AP 250, AST
    22, ALT 23, T bil 0.4. She’s
    asymptomatic. Differntial includes
       Acute Fatty Liver of Pregnancy (AFLP)
       HELLP
       Pre-eclampsia
       Hepatitis
       None of the above
AFLP

   Presents in 3rd trimester with
    malaise, headache, nausea, poor
    appetite, abd pain
   Moderate elevations of
    transaminases
   Incr PT
   With early detection, mother
    survival>90%, infant>60%
HELLP

   Hemolytic anemia
   Elevated Liver enz
   Low Platelets
   More severe variant of pre-
    eclampsia/eclampsia
Pre-eclampsia/Eclampsia

   Hypertension
   Edema
   Proteinuria
   With or without sz
Now Some Pictures
Barrett’s esophagus
Achalasia
Esophageal ulcer
PSC
Peutz-Jeghers syndrome
Acanthosis Nigricans
E. Nodosum
Pyoderma Gangrenosum
Anal Crohn’s
Crohn’s fistulas
Dupuytren’s contractures
Porphyria Cutanea Tarda
UC
Crohn’s
Radiation colitis
Dermatitis Herpetiformis
Celiac Sprue
Finally some questions from the board
   Diarrhea with dairy products
       Lactose deficiency


   D-xylose test positive, diarrhea,
    steatorrhea
       Small bowel biopsy r/o celiac
   Diarrhea, malabsorption, s/p
    radiation
       Radiation enteritis


   Duke C
       Chemotherapy


   IBS associated
       Child abuse
   UC with abnormal LFT
       ERCP


   Cholangitis
       ERCP


   FAP
       Colectomy
   Colonoscopy 2 adenomatous polyps
       Repeat in 3 years


   Dysphagia after long term heart
    burn
       Stricture, PPI forever


   Meds working immediately in
    Crohn’s
       Budesonide (?)
   AST, ALT in the thousands
       Acute hep, ischemic hep, drug toxicity


   Post exposure prophylaxis for hep B
       Immunoglobulin


   Hep B
       PAN
   PBC
       Send for liver transplant


   Cimetidine
       Interacts with theophylline


   Activity of hep B
       Hbe Ag
   Trt of diarrhea in carcinoid
       Octreotide


   Periumbilical pain after Afib
       Small bowel infarction


   Gastroparesis
       Control blood sugar
GOOD LUCK FOR THE BOARDS

								
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