Download distinguish between each of the disorders (compare and contrast

29 Noninfectious Hepatitis and Hepatic Obstruction – distinguish between
each of the disorders (compare and contrast epidemiology, symptoms, labs,
treatments)
Increased Production of Bilirubin
Unconjugated Bilirubin (IB)
 Increased production  hemolysis (extravascular and intravascular), clotting disorder,
transfusion and transfusion reaction, sepsis with DIC, severe burns
 Decreased uptake
o Dec uptake of IB bilirubin  CHF, Drugs (rifampin, probenecid)
o Dec ability to conjugate bilirubin  Gilbert’s Syndrome, Crigler-Najjar Syndrome,
Neonatal jaundice, Hyperthyroidism, Estrogens, cirrhosis, hepatitis, Wilson’s disease
Conjugated Bilirubin (DB)
 Intrahepatic Cholestasis (impaired excretion)  hepatitis (viral, alcoholic, non-alcoholic),
Hepatocellular injury (arsenic, acetaminophen overdose, chlorpromazine), Primary Biliary
Cirrhosis, End stage liver disease, sepsis, TB, amyloid, sacroidosis, lymphoma, Sickle Cells disease
(liver crisis), Budd-Chiari Syndrome
 Extrahepatic Cholestasis (obstruction)  cholelithisis, tumors, strictures, acute and chronic
pancreatitis, PSC, ascaris lumbricoides, liver flukes
↑Unconjugated
due to
↑production
↑ Unconjugated
due to↓conjugation or
↓transport
↑ Conjugated due to
Impaired excretion
(Intrahepatic)
↑ Conjugated due to
biliary obstruction
(Extrahepatic)
Hemolysis &
hemoglobinopathy
Gilbert’s disease or CriglerNajjar Syndrome
Rotor’s or
Dubin Johnson syndrome
Cholelithiasis
(stone)
Transfusions and
transfusion reaction
Physiologic: Neonatal and
Pregnancy
Cirrhosis
Stricture
Burns or crush
injuries
Cirrhosis
Cancer
Cancer
Sepsis
Hepatitis
Hepatitis
Chronic pancreatitis
Drug inhibition (Rifampin
and probenecid)
Amyloidosis
Primary Sclerosing
Cholangitis
Drugs that Cause Hepatotoxicity:
 Acetaminophen, indomethacin, ketoconazole, carbamazepine, ranitidine, allopurinol, isoniazid,
phenytoin, atenolol, diltiazem, naproxen (NSAIDs), penicillin, para-aminosalicylic acid,
sulfonamides
Drugs that Cause Intrahepatic Cholestasis
 Erythromycin, amoxicillin/clavulanate, cyclosporine, enalapril, ketoconazole, oral
contraceptives, tamoxifen, methylestosterone, thiabendazole
Neonatal Jaundince
 Physiologic jaundice, Breast feeding (fatty acids in breast milk inhibit hepatic conjugation), Rh
incompatibility
 Tx: Phenobarbital and Phototherapy
Crigler-Najjar Syndrome Type I
 UGTI1A1 expression not present, Autosomal recessive, serum bilirubin >345 µmol/L

Tx: Phototherapy, transfusions, heme oxygenase inhibitors, oral calcium phosphate and
carbonate (form bilirubin complexes), liver transplantation; treatment with phenobarbital is
NOT EFFECTIVE
Crigler-Najjar Syndrome Type II
 UGT1A1 reduced levels (<10% of normal), Autosomal recessive, serum bilirubin <345 µmol/L,
kernicterus is rare, bile is pigmented, monoconjugates = largest fraction of bile conjugates
 Tx: Phenobarbital (dec 25% of bilirubin), Phototherapy
Gilber’s Disease
 Common (10% of jaundice causes), unconjugated hyperbilirubinemia, Autosomal recessive,
reduced activity of glucoronyltransferase
 Symptoms: Symptoms include a (non-itching) jaundice, fatigue, made worse by stress,
exertion, not eating, alcohol, dehydration or infection.
 Tx: not required; normal life expectancy; avoid extreme exertion, alcohol, drugs
Dubin Johnson’s Syndrome and Rotor Syndrome
 Both: Autosomal recessive, inc conjugated bilirubin, made worse by alcohol, hepatitis, drugs
excreted in liver, OC, pregnancy, infection, No treatment required
 Dubin Johnson’s: abnormal canulicular transport gene, BLACK pigmentation of liver biopsy,
Gallbladder CANNOT be visualized, urine corporphyrins >80% isomer 1
 Rotors: unknown gene mutation, NORMAL liver biopsy, Gallbladder CAN be visualized, Urine
Corporphyrins <70% isomer 1
Cirrhosis
 Inflammation and repair  scar tissue inhibits regeneration liver cells form nodules
 Liver Chapman Pt: 5-6th Right Anterior Intercostal Space
 Causes: Hemochromatosis: AR, Iron accumulation in liver/tissue/organs. Hemosiderosis:
excessive transfusions, Siderin accumulation in organs, Reversible with chelation. CF, Alpha 1
Antitrypsin Deficiency, PBC, PSC, Wilson’s disease, Alcohol, medication, chronic viruses,
autoimmune disease, chronic CHF, schistosomiasis
 Signs and Symptoms: Jaundice, fatigue, weakness, loss of appetite, itching, bruising. Late Nonspecific symptoms
 Complications: kidneys retain Na and H20  ascites  Spontaneous bacterial peritonitis,
scarring  portal hypertension, Esophageal varices, ammonia accumulation hepatic
encephalopathy, drug toxicity, hypersplenism, hepatorenal syndrome (late stage), liver cancer
 Diagnosis: Initial elevation of liver enzymes (later falling), liver biopsy (scarring and nodules), CT
 Tx: Alcohol reduction, avoid iron, copper (if genetic) and toxic drugs, treat ascites
Primary Biliary Cirrhosis
 Autoimmune disease that destroys intrahepatic bile ducts, FEMALE, fatigue and pruritus,
Elevated AMA, ALP, GGTP, treat with liver transplant
Primary Sclerosin Cholangitis
 Inflammation of intra and extrahepatic bile ducts, associated with UC, MALE, elevated p-ANCA
autoantibody, Diagnosed with MRI, treat with liver transplant
Primary Ascending Cholangitis
 CHARCOT’S TRIAD: RUQ pain, fever, jaundice
 Bacterial infection usually from gallstone
o Aerobes: E. Coli, Klebsiella, Pseudomonas *
o Anaerobic infection Bacteroides fragilis and Clostridium perfringens

Diagnosis: CBC  leukocytosis, Do electrolyte panel, pancreatitis  hypocalcemia, liver tests 
hyperbilirubinemia and high ALP, Normal PT/PTT UNLESS sepsis, high CRP and ESR, Bile duct
stone  inc pancreatic enzyme, Do Biliary Culture at time of surgery
 Imaging: US (early), CT or MRI, ERCP diagnostic AND therapeutic
 Tx: Resuscitation with electrolyte and IV fluids, NPO, and nasogastric tube, Parenteral broad
spectrum antibiotics (response rate 80-90%), biliary decompression with ERCP, sphincterotomy,
percutaneous drainage in severely ill pts,
Pancreatic Tumors
 Tumors of the head of pancreas (most common tumor of pancreas)  painless jaundice in pts
over 50; alcohol and tobacco inc risk of pancreatic cancer
 Asymptomatic until jaundice  metastatic at time of diagnosis; 85% aggressive
adenocarcinoma, 15% other (respond better to treatment)
 Tx: Whipple’s procedure for tumors at head of pancreas, distal pancreatectomy for tumors of
tail
30 Cholelithiasis, Cholecystitis, Choledocholithiasis and Cholangitis


Identify the typical presentation of a patient with gallbladder disease

Cholesterol, pigment, mixed types

Saturation, stasis, nucleating factors

Age, gender, obesity, exogenous estrogen, vagotomy, pregnancy, hemolysis, cirrhosis, E. coli

RUQ pain, elevated bilirubin, jaundice
Differentiate between biliary colic (symptomatic cholelithiasis), cholecystitis, acalculous
cholecystitis, choledocholithiasis and cholangitis


Biliary colic (symptomatic choleithiasis) aka gallstones
o
Fat, fertile, forty (saturation, stasis, nucleating factors)
o
Only 20-30% of gallstone pts get sx, and only 1% develop complications
o
Diffuse pain
o
Complications = chelecystis, cholangitis, gangrenous GB, GB wall perforation w/
abscess, gallstone pancreatitis, bilioenteric fistula (GB wall fuse w/ duodenum),
gallstone ileus
Cholecystitis (inflammation of the GB)
o
Old men, surgical-related, DBM
o
Acute - usually from impacted stone in neck or cystic duct
o

Most have bacterial infection

Localized RUQ pain, + murphy's sign (inspiratory arrest w/ deep palpation in RUQ)

Get ECG, CXR (to r/o something worse), US, CBC, amylase, liver profile

Tx - IV ABX, surg
Chronic - repeated bouts of biliary colic and/or acute cholectysitis -> GB wall
inflammation and fibrosis





Best imaging = US (thickened GB wall and contraction of GB w/ stones in
advanced dz)
acalculous cholecystitis (no-stones; only in 5% of acute cholectystis; but is life-threatening)
o
Prolonged fasting, immobility, hemodynamic instability, AIDS (CMV, cryptosporidium)
o
From GB stasis and ischemia
o
US = absence of gallstones, thick GB wall
o
Tx = broad spectrum ABX, drainage, cholectystectomy
Choledocholithiasis (stones pass into common bile duct)
o
<3mm - passes; >3mm - obstruct sphincter - jaundice
o
Gallstone pancreatitis in < 15% of pts w/ symptomatic gallstones
o
Best seen with ERCP cholangiography (see CBD stones)
Cholangitis (infected bile sitting behind duct, leaking into liver)
o
Jaundiced, bacteremia through portal traid -> sepsis ensues
o
Charcot's triad - RUQ pain, fever, jaundice
o
Reynold's pentad - RUQ pain, fever, jaundice, mental status chain, hypotension
o
Surgical emergency!!
o
Tx - resuscitation, IV ABX, US, ERCP, PTC if obstruction seen on US
Recognize the evaluation and treatment of patients with gallbladder disease


Evaluation
o
Plain radiograph - not test of choice, may see gallstones, may be normal, may see air in
GB (mostly used to r/o other causes)
o
Ultrasound - is the mainstay (cheap, bedside, specific, sensitive, can see gallstones)
o
CT - Consider CT if indicated for other things (ischemic colon, obstruction, US is missing
info, perforation, abscess) - to r/o other things or gain info. Or if US is difficult w/
obesity
o
Scintigraphy (HIDA scan) - only if common bile duct and cystic duct are patent, doesn't
ID stones, estimates GB fxn after via EF CCK admin, biliary dyskinesia when GB has pain
w/o stones or EF < 30%
o
Cholangiography - to view the bile duct (best for this), MRC and CT are noninvasive,
ERCP and perc. transhepatic are invasive. ERCP most useful for hepatobiliary
malinancies and choledocholithiasis. Pt requires anesthesia, can puncture things.
o
Lab tests - bilirubin (conjugated and non-conjugated), alkaline phosphatase, ALT/AST in
serum
Treatments
o
Cholecystectomy (GB removal) usually laparoscopic- indicated 24-72 h for acute
cholecysitis, empyema or perforation of GB, previous choledochithiasis w/ endoscope
duct clearance

o

Elective - biliary dyskiniesa, chronic cholecystis, symptomatic cholelithiasis
Intraoperative cholangiogram - indicated if pre-op ALT/AST are elevated, unclear
anatomy, dilated CBD, jaundice, gallstone pancreatitis
Recall risk factors for cholangiocarcinoma

Painless jaundice, dismal prognosis, direct hyperbilirubinemia

DX - US (dilated ducts), ERCP (location, tissue sample, drainage), three-phase CT (evaluate
resectability)

TX - palliation (bile duct drainage - ERCP, PTC), no role for chemo/radiation

RF = choledochoal cysts, liver flukes (clonorchis and opisthorchis), recurrent pyogenic
cholangitis
o
CHRONIC REPETITIVE INFLAMMATION!!!!!!
31-32 Hepatitis
Infectious Hepatitis is generally caused by one of the major Hepatitis viruses
 General features include Necroinflammation of the hepatocytes via T-CELL RESPONSE
Hepatitis A
 HAV presents as Self-limiting disease
 Increased risk with: travelers, homosexuals, IV drug users, Clotting factor disorders, working with
non-human primates
 Incubation: 28 days (15-50 d range)
 Transmission: FECAL-ORAL; person-person; contaminated food/water
 Replicates in liver -> shed in feces from ~2 weeks with onset of clinical illness
 Immunity: See IgG Antibodies
 Young children (<6) may asymptomatic -> makes them carriers
o
o


Abrupt onset presenting with jaundice, fever, fatigue, dark urine, abdominal pain
Can also cause arthralgia and rash; severe forms can lead to fulminant hepatic failure or
autoimmune hepatitis
Treatment: Prevention
o Vaccine: 2 dose series (0 + 6-12 months)
Serologic Testing:
o IgM HAV (acute infxn)
o IgG HAV (lifelong immune);
o Inc ALT (non-specific)
Hepatitis B
 Caused by infection by HBV via percutaneous or mucosal contact with infectious blood or body
fluids -> NOT through food/water, sharing utensils, breastfeeding, kissing/hugging, or
sneezing/coughing
 Incubation: 6wks - 6 months
 Risk factors: Infants born to infected mothers; infected sex partners; IV drug users; health
care/safety workers; travelers
 Treatment: Prevention via Vaccine (FOR EVERYONE) and safety precautions
 Symptoms: Fever, fatigue, loss of appetite, N/V, Dark urine/Clay-colored stools; jaundice
 Acute complications: Fulminant hepatitis; Chronic: Hepatocellular carcinoma
 Serologic testing:
 HBsAg: surface antigen detected in acute or chronic infections  shows active
infectious process
 Anti-HBs = antibodies to surface antigen produced after acute infection OR indicate
effective vaccination
 NEGATIVE during acute infection (sometimes antibodies not created until after
resolution of acute infection)
 Total Anti-HBc: IgM, IgG, antibodies to core antigen produced in response to past
infection start appearing at onset and persist for life
 IgM anti-HBc: IgM presents at first and then fades as IgG appears and persists
for life
 HBeAg: positive in the incubation and acute phase
 Anti-Hbe: virus is rapidly reproducing either during chronic phase at peak episodes of
reactivation or during acute phase

Hepatitis D
 HDV requires HBV to replicate thus is transmitted in similar fashion
 Risk factors: IV drug users
 Infection with HDV can increase risk of fulminant hepatitis from HBV
 Tx: Prevention with HBV vaccine
Hepatitis C
 Caused by HCV infection
 Risk factors: current or previous IV drug users; Recipients of clotting factor concentrates made
before 1987; Recipients of blood transfusions or solid organ transplants before July 1992; Chronic
hemodialysis patients
o Health care workers after needlesticks; Recipients of blood or organs from a donor: Persons
with HIV infection; Children born to HCV-positive mothers
 Incubation: 8 weeks (2-24wks)
 Transmission: Percutaneous exposures, IV drug use (common), Sex with HCV Positive person,
Sharing personal items contaminated with blood
 SCREENING FOR PATIENTS BORN FROM 1945-1965
 Symptoms: Acute (25% patients) -> jaundice, fever, fatigue, Clay colored stools or dark urine; Also
see arthralgia, paresthesia, myalgia, pruritis, Sicca syndrome, and sensory neuropathy
 Complications include DM (3x increased chance), Glomerulonephritis
o 75-85% develop chronic infection
o 60-70% develop chronic liver disease
o 5-20% develop cirrhosis within 20-30 years
o 1-5% Die from consequences of chronic infection
 Diagnosis: serum testing of elevated liver enzymes, ANA, Rheumatoid Factor, Anticardiolipin
antibodies, cryoglobulins, and Anti-HCV (test of choice)
o Qualitative tests: HCV RNA PCR (if Anti-HCV is positive)
 If negative Anti-HCV -> sample is nonreactive; but test PCR if recent exposure is
suspected
 Positive Anti-HCV -> presume infection
 Positive Anti HCV and Negative PCR -> No infection
 Positive Anti-HCV and Positive PCR -> infection
Quantitative tests: Titer of HCV RNA PCR
Treatment: Prevention and assess for chronic liver dz
o Genotyping for protease and polymerase inhibitors may determine length of treatment and
response rate of treatment
o Counseling to avoid alcohol, avoid medications metabolized in liver (acetominophen)
o Highest Priority patients are those with advanced fibrosis; severe extrahepatic hepatitis;
compensated cirrhosis; or liver transplant recipients. Also patients high risk for liver related
complications and severe Hep C complications
o Treatment decisions should balance the anticipated reduction in transmission vs. the
likelihood of reinfection in patients whose risk of HCV transmission is high and in whom HCV
treatment may result in a reduction in transmission
o

Hepatitis E
 Caused by HEV infection as self-limited infection
 Mostly found in developing countries especially with Young adults (15-40 years) and PREGNANT
WOMEN (30% -> risk of death in 3rd trimester)
 Transmission: Fecal-oral transmission
 Symptoms: 50-90% are asymptomatic and can mimic other viral hepatitis symptoms
 No diagnostic tools -> clinical presentation with recent travel to endemic areas
 Treatment: Prevention/sanitation
-> CASE STUDIES FROM CDC
33 Pancreatic Tumors
Pancreatic Neuroendocrine Tumors (pNET)
Insulinoma
 Presentation - 45 yo, hyper-attenuating lesions that are vascular on CT/MRI
 DX - CT/MRI, endoscopic ultrasound (EUS), mass anywhere in pancreas; avg size 1.0-1.5 cm
 HX - most are benign
 TX – resection (best) /enucleation
 Whipple Triad:
o Fasting neuroglycopenic symptoms
o Low Blood Sugar (40-50 mg/dL)
o Relief of symptoms with glucose administration
VIPomas
 Presentation - rare, WDHA syndrome (watery diarrhea, hypokalemia, achlorhydira), vernerMorrison syndrome (diarrhea, high level VIP > 500, pancreatic tumor), most are malignant
 DX - CT/MRI, endoscopic ultrasound (EUS), mass in body/tail, somatostatin receptor scintigraphy
 HX - most malignant
 TX - resection/debulking, somatostatiin analogue (octreotide) to block sx in malignant pts
Glucagonoma
 Rare, Women, arise from alpha cells, 4 Ds (diabetes, dermatitis, DVT, depression), Diagnosis: CT/
Presentation - rare, women, from alpha cells, 4 D's (DBM, dermatitis [necrolytic, migratory
erythema], DVT, depression)
 DX- CT/MRI/EUS, large size 5-10 cm
 HX - most are malignant
 TX - resection/debulking/octreotide
Somatostatinoma
 Presentation - rare, steatorrhea, DB, hypochlorohydria, gallstones
 DX - fasting somatostatin level >14
 HX - head of pancreas solitary tumor >2 cm, 90% malignant with high metastases potential,
 TX - resection/debulking
Pancreatic Cystic Neoplasms
Serous (cystadenoma, cystadencarcinoma)
 Presentation - 60-70 yo, found incidentally, vague sx (pain, early satiety, jaundice)
 DX - CT/MRI/EUS, located in head of pancreas, "sunburst appearance", low CEA, mucin, and
amylase on fluid analysis
 HX - majority are benign
 TX - observation (<4cm, asymptomatic), resection (>4cm, symptomatic or uncertain)
Mucinous (cystadenoma, cystadencarcinoma)
 Presentation - women, 5th decade, some pts have abd pain, from mucinproducing epithelium ovarian-like stoma
 DX - CT/MRI, body/tail > head of pancreas, "egg-shell" calcification, simple
cyst, solid components = malignancy, EUS, fluid analysis (+ mucin, elevated
CEA, low amylase)
 HX - most are malignant
 TX - resection is preferred
Intraductal Papullary Mucinous Neoplasm (IPMN): Side branch vs Main Duct
Cystic mucinous neoplasm of pancreatic duct, presents in 6-7th decade, cancers range
from benign  carcinoma in situ, abd pain, weight loss, new onset diabetes, early
satiety
Side Branch
 Focal, single side branch, multifocal, multicystic, risk of malignancy inc with
size of cyst, Diagnose: CT/MRI/EUS w/ FNA, malignancy risk 10-15%
 Tx: Observe and surveillance for cysts <3 cm with low CEA (<200 ng/mL) and
resection for >3 cm cysts with high risk features (partial pancreatectomy),
Main Branch
 Diffuse dilation on pancreatic duct, columnar metaplasia w/ thick
mucinous secretions (ERCP shows oozing mucin in ampulla of Vater),
EUS w/ FNA shows elevated CEA (>200 ng/mL) and mucin, 30-50% risk
of malignancy
 Tx: partial pancreatectomy favored over total pancreatectomy
Mucinous
Multicystic side branch
IPMN
Main Branch IMPN CT
Pancreatic Cancer (adenocarcinoma)
 Presentation - very common (4th most common CA deaths/y), men, 72
yo
o Head of pancreas - wt loss, jaundice, pain (late SX), palpable distended gallbladder w/o
pain (Courvoisier sign)
o Body/tail - wt loss, pain, early satiety, new onset DB




Risk factors - smoking (most common), age, chronic pancreatitis, obesity, DB, hereditary 
Peutz-jegher's (STK11), Cystic fibrosis (CFTR), Lynch syndrome (MLH1), FAP (APC), Familial
pancreatitis (PRSS1)
DX - elevated bilirubin/alkaline phosphatase, decreased
albumin/pre-albumin, elevated CA 19.9 (very sensitive/ not
specific),
CT: double duct sign - bile duct and pancreatic duct both dilated,
lymphadenopathy, liver metastases, ERCP (ductal brushings, biliary
decompression/stenting), EUS (relationship of tumor to SMV/SMA,
biopsy with high accuracy rate)
TX - staging (TNM), NCCN (to determine resectable vs. unresectable)
o Types = metastic (most common), locally advanced
resectable, borderline resectable, resectable
o Resectable (early) - surgery with adjuvant chemotherapy, diagnostic laparoscopy,
pancreaticoduodenectomy (whipple operation) at head of pancreas, pancreatectomy
for body/tail
 Whipple operation complications - delayed gastric emptying, fistula, infection,
abscess
o Locally resectable (borderline resectable) - neoadjuvant chemo up to 6 mo -> radiation
-> restaging -> consider surgery (early surgery can create a fibrotic zone)
o Unresectable (late) - chemo only
34 Pancreatitis


Correlate the anatomy of the pancreas to the pathophysiology of pancreatitis
 Endocrine pancreas - insulin secretion - goes to the systemic blood supply
 Exocrine pancreas - digestive enzymes - goes to the pancreatic ducts (excreted via acinar
cells)
 Parts = Head, body, tail, Uncinate process
 Minor pancreatic duct/sphincter/papilla; major pancreatic duct/sphincter/papilla
o Ampulla of Vater
 Blood supply
o Near the splenic vein which can cause terrible complications if nicked during surgery
o Branches of hepatic a., gastro-omental a., gastroduodenal a. SMA, superior pancreatic
duodenal (anterior/posterior), inferior pancreatic duodenal (anterior/posterior)
List the etiology, presentation, workup and management of patients with both acute and chronic
pancreatitis
 Acute pancreatitis
o Etiology - gallstones (most common), etOH (2nd most common), ERCP, drugs,
anatomic obstruction, idiopathic, autoimmune pancreatitis
o Pathophysiology - irritative etiologies cause pancreatic injury (to pancreatic duct) ->
TNF-alpha and IL-1 -> inflammatory cascade (cytokines) -> systemic inflammatory
response syndrome (SIRS) -> multi-organ dysfunction syndrome -> death
 SIRS = the body attacking itself
o Presentation - Nausea/vomiting is associated with the pain which is constant, localized
to the upper part of his abdomen, and radiates to the back. May be associated with
etOH.
o Work-up - physical exam, labs (for Ranson's criteria), ultrasound of RUQ (to r/o GB
problems), liver function tests




etOH pancreatitis = DX of exclusion (r/o other causes)
Gallstone pancreatitis = increased bilirubin, increased Alk Phosph, stones on US
o TX - (based on etiology)
 For etOH pancreatitis - start resuscitation (IV fluids, urine output monitoring w/
folly catheter), stop drinking
 For gallstone pancreatitis - ERCP, gallstone removal
 Chronic pancreatitis
o Etiology - etOH, autoimmune, tropical (less common in US), smoking, anatomic
(pancreatic divism), idiopathic
o Pathophysiology - repeated bouts of acute pancreatitis and autodigestion of pancreas
from trapped digestive enzymes and may lead to infection
o Presentation - PAIN, DB, stenosis of distal common bile duct, +/- fever, +/- drinking
o Workup - includes CT to view pancreas (black stuff indicates air)
o TX - pain control, control etiology (e.g., stop drinking, fix pancreatic divism)
 Infected pancreas = resuscitate (IV fluids, urine monitoring), aspirate, get
cultures, debridement
Recall the modified **RANSON'S CRITERIA** and their related prognostic indicators
 On admission first 24 hours (each worth a point) --- "GA LAW"
o Blood Glucose > 200 mg/dL
o Age in years > 55 years
o Serum LDH > 350 IU/L
o Serum AST > 250 IU/L
o White blood cell count > 16000 cells/mm3
 At 48 hours (each worth a point) --- "C HOBBS"
o Calcium < 8.0 mg/dL
o Hematocrit decrease > 10%
o PO2 < 60 mmHg
o BUN increase >5 mg/dL after IV fluid hydration
o Base deficit (negative base excess) > 4 mEq/L
o Sequestration of fluids > 6 L
 Mortality correlates w number of criteria present.
o 0-2 <5% mortality
o 3-4 15%
o 5-6 40%
o 7-8 100%
Recognize the most common complications of pancreatitis
 Infection, death
35 Gluten, Dairy, and Probiotics
Gluten
 Peptide fractions of proteins (prolamines) found in wheat (glutenin, gliadin), barley (hordein,
and rye (secalin); gives elasticity to dough and helps it rise
 Found in couscous, barley, rye, triticale, wheat, durum flour, farina, beer, pastas, crosscontamination when gluten free foods contact gluten containing foods,
Gluten Allergy
 IgE Mediated Allergy to ay grains containing gluten; Wheat is common
Gluten Sensitivity
 Nausea, abd pain, diarrhea in response to dietary gluten,
 Negative eval medically: non-celiac gluten sensitivity (no immune response)
 Tx with Gluten free diet
Celiac Disease
 Peptides reach SI  travel out of the lumen  across epithelia to the lamina propria 
inflammatory response
 Injury to SI  flattened villi and elongation of crypt cells  loss of absorptive surface and
reduction of enzymes  impaired absorption of macro/micronutrients (fat soluble vitamins,
iron, B12, and folic acid)  net secretion of fluid  diarrhea
 Most common cause of chronic malabsorbtion causing weight loss, pain and bloating
 Testing: TTG antibody (IgA anti-tissue transglutaminase) in pts >2; Children <2 test IgATTG
with Deaminated gliadin peptides IgA and IgG
o To test for gluten sensitivity pt MUST be on gluten containing diet
o Test pts with Type I DM, family member with celiac, pt with elevated serum
aminotransferase with unknown etiology
o HLA-DQ2/DQ8 genotyping not routine for initial dx but can RULE OUT celiac
Diary Allergy
 IgE mediated reactions: food induced anaphylaxis, oral allergy syndrome/ pollen food syndrome,
immediate GI hypersensitivity, food dependent exercise induced anaphylaxis
Lactose Intolerance
 Malabsorbtion of dietary lactose in SI resulting in bloating, abd pain, diarrhea (unabsorbed
lactose causes osmotic diarrhea), and flatulence (caused by fermentation of unabsorbed lactose
by gut bacteria)
 Lactase located in brush border of SI  hydrolyzes lactose into glucose and galactose for
transport
 Lactase deficiency: 1° adult hypolactasia (down regulation of enzyme) is most common, injury to
SI brush border (infection, inflammation, malnutrition) is second most common, congenial
alactasia is rare cause
 Typically loose lactase by 90% after age 6; Asians and American Indians loose 100% of lactase,
Ashkenazi Jews and Blacks loose 60-80%, Latinos loost 50-80% Northern Europeans loose 2%
 Symptoms occur in 2 hrs; pts can still consume 8-12 oz of milk; Yogurts with live cultures contain
bacterial derived lactase
Indication and Mechanism for Probiotics
 Live microorganisms that bebefit the host when administered in adequate amounts
 Ex: Lactobacillus (L. acidophilus, L. rhamnosus, L. bulgaricus, L. reuteri, L. casei) Bifidobacterium
sp., and Saccharomyces boulardii, a nonpathogenic yeast
 Mechanism: direct competition btw pathogenic bacteria in gut and immune modulation and
enhancement
 Indications:
o Reduce risk of antibiotic associated diarrhea (start within 72 hrs of antibiotics)
o Dec duration and risk of acute infectious diarrhea (viral and traveler’s)
o IBS- lacks evident but some decreased symptoms of abd pain and bloating
o Reduce the dietary antigen load by degrading and modifying macromolecules in the gut
o Atopic dermatitis: downgrade the excessive immune response to foreign antigens that
lead to atopic dermatitis’ prophylaxis
o Firm evidence lacking: H pylori infections, IBD, URI
o
Reverse inc intestinal permeability characteristic of children with food allergy and
enhance specific IgA responses