hepatology

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hepatology

• A
• Guide
• To commonly used
• Liver tests

2

• Context dependent
• Types of history questions asked
• Algorithms not useful
• Requires critical thinking

3
ISOLATED ABNORMALITIESIN LIVER TESTS

• bilirubin liver/ ?
• aspartate transaminase (AST, serum
  glutamic-oxaloacetic transaminase SGOT) liver
  cell
• alanine transaminase (ALT, serum
  glutamic-pyruvic transaminase SGPT) Liver Cell
• gamma-glutamyl-transpeptidase (GGTP) chemical
  injury to liver cell
• alkaline phosphatase (ALP) Bile canal/?
• lactate dehydrogenase (LDH)
• liver cell/?

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Nonhepatic Sources of Abnormalitiesfor Selected Laboratory Tests Nonhepatic Sources of Abnormalitiesfor Selected Laboratory Tests
Test Non Hepatic Source
Bilirubin Red blood cells (eg, hemolysis, intraabdominal bleed/hematoma)
AST Skeletal muscle, cardiac muscle
LDH Heart, red blood cells
Alkaline phosphatase Bone, first trimester placenta, kidney, intestines
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EVALUATION OF LIVER DISEASEBASED ON ENZYMES

• Liver disease categories-
• hepatocellular, in which primary injury is to the
  hepatocytes
• cholestatic, in which primary injury is to the
  bile ducts and
• infiltrative, in which the liver is invaded or
  replaced by nonhepatic substances such as
  neoplasm or amyloid

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Why this torture?

• often makes subsequent evaluation faster and more
  efficient!

7

• AST, ALT
• hepatocellular
• and
• alkaline phosphatase tests
• cholestatic
• are most useful to make the distinction between
  hepatocellular and cholestatic disease.

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ASTALP

• a patient with an AST of 120 IU/ml (normal up to
  40) and an alkaline phosphatase of 130 IU/ml
  (normal up to 120).
• This pattern is
• hepato cellular and
• not cholestattic (mild alp increase)

9
Serum aminotransferasesALT (SGOT) and AST (SGPT)

• measures of liver cell injury
• AST is less liver-specific than the ALT
• viral hepatitis (primarily affect hepatocytes)
• will cause disproportionate elevations of AST and
  ALT compared to alkaline phosphatase

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• In patients with alcoholic hepatitis
• AST/ALT ratio
• usually greater than 2 and the AST is 400 IU/mL
  or less

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MILD AST/ALT Increase in

• fatty liver disease
• seen most often in those with
• obesity
• diabetes or
• elevated blood lipids
• Fatty liver is also seen on those who drink
  alcohol

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ALP

• most densely represented near the bile
  canalicular membrane
• obstructive diseases affect hepatocyte secretion
• Increase seen in
• Bile duct obstruction,
• primary sclerosing cholangitis,
• and primary biliary cirrhosis

13
Category of Liver Disease by Predominant Serum Enzyme Abnormality Category of Liver Disease by Predominant Serum Enzyme Abnormality Category of Liver Disease by Predominant Serum Enzyme Abnormality Category of Liver Disease by Predominant Serum Enzyme Abnormality
Test Liver Disease Category Liver Disease Category Liver Disease Category
Test Hepato-cellular Cholestatic Infiltrative
AST, ALT higher than alkaline phosphatase Typical      
Alkaline phosphatase higher than AST, ALT    Typical   
Elevation of alkaline phosphatase with near-normal AST, ALT    Typical Typical
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Alp elevation

• Canalciaular obstruction by cholestatsis ?
• Or
• Liver infiltration by metastasis?

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? differentiate

• requires imaging studies of the liver
• ultrasound,
• computerized tomography, or
• magnetic resonance imaging most often identifies
  tumor infiltration of the liver

16
?differentiate

• cholangiography
• (E ndoscopic Retrograde Cholangio Pancreaography)
  ERCP
• Useful for bile duct obstruction cholestasis

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BILIRUBIN ELEVATIONS Facts

• normal breakdown of pigment- containing protein
  hemo and myo globin
• tightly albumin-bound, is delivered to the liver
  
• efficiently extracted and conjugated by hepatic
  glucuronidation and sulfation.
• Conjugated bilirubin is rapidly excreted into
  bile and removed from the body through the gut
• amount of conjugated bilirubin present in serum
  in healthy subjects is trivial (less than10 of
  measured total bilirubin).

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• An elevated level of conjugated serum bilirubin
  implies liver disease.
• Because only conjugated bilirubin appears in
  urine,
• The finding of bilirubinuria
• also implies liver disease.

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Terminology!
Bilirubin Fractions Present in Blood and Urine Bilirubin Fractions Present in Blood and Urine Bilirubin Fractions Present in Blood and Urine Bilirubin Fractions Present in Blood and Urine
   In SerumAs Measured As Presentin Urine
Un- Conjugted (fat soluble) Albumin bound Indirect Reacting bilirubin (90) Never
Conjugated (water soluble) Unbound Direct Reacting Bilirubin (10) Yes, when serum bilirubin exceeds 3-4 mg/dL
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hepatitis

• Hepatitis a

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Hepatitic viruses

• A, B, C, D, E ARE PRIMARY HEPATITIS VIRUSES
• EBV, AND CMV CAUSE HEPATITIS BUT NT PRIMARY LIVER
  VIRUSES

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HAV

• RNA VIRUS
• fecal-oral TRNSMISSION
• annual incidence is 9.1 per 100,000
• RAW OR PARTIALLY COKED SHELL FISH
• High Risk Group Travelers / Day-Care children /
  Sewage workers / Male homosexuals / IV drug users
  /

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SIGNS AND SYMPTOMS

• Incubation 15-49 days ( 25)
• fatigue, weakness, anorexia, nausea, vomiting,
  abdominal pain
• Followed by jaundice within 2 weeks (70)
• Hepato splenomegaly and cervical lymphadenopathy
  / -
• Infective period 3 weeks prior to jaundice and
  up to 8 days after jaundice clears

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DIAGNOSIS

• Detecting IgM anti-HAV in the serum
• Presence of IgG anti-HAV assesses immunity
• THERAPY
• self-limited infection
• PREVENTION
• Havrix is recommended as two injections 6 to 12
  months apart
• Full recovery in 2 months

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hepatitis

• Hepatitis b

27
Epidemiology

• 1.25 million people infected (CDC)
• 350 million people carriers worldwide (5)

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HBV Virus

• Double shelled virus particle
• Outer envelope of hepatitis B surface antigen
  (HBsAg)
• Inner nucleocapsid of core antigen (HBcAg)

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Natural History of HBV

• can survive outside the body for up to 1 week
• spread predominantly
• parenterally
• through intimate personal contact and
• perinatally
• At risk
• intravenous drug users
• children of mothers with HBV
• men who have sex with men
• patients on hemodialysis and
• those exposed to blood or blood products

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Natural History of HBV

• incubation period 45 to 160 days (100)
• Usually mild illness (30-50)
• Fulminant (0.1-0.5)
• Insidious onset of nausea, anorexia, malaise and
  fatigue, or flu-like symptoms, pharyngitis,
  cough, coryza, photophobia, headache, and
  myalgias
• may precede the onset of jaundice
• Mild enlargement and slight tenderness of the
  liver, mild splenomegaly, and posterior cervical
  lymphadenopathy (15 to 20 )

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extra-hepatic manifestations

• arthralgias,
• Glomerulonephritis (children) and
• polyarteritis nodosa
• Chronic infection (or the carrier state), defined
  as the persistence of HBsAg in the blood for more
  than 6 months

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Viral Markers

• first detectable viral marker is HBsAg
• followed by hepatitis B e antigen (HBeAg)
• HBV DNA
• HBV DNA and HBeAg levels begin to fall at the
  onset of illness
• Core antigen does not appear in blood, but
  antibody to this antigen (anti-HBc) is detectable
  with the onset of clinical symptoms

34
Viral Diagnostics of HBV

• immunoglobulin M (IgM) diagnostic assay for
  acute hepatitis B infection.
• Anti-HBsAb is a long-lasting antibody and is
  associated with immunity
• presence of anti-HBsAb and anti-HBcAb (IgG)
  indicates recovery and immunity in a previously
  infected individual
• a successful vaccination response produces
  antibody only to HBsAg
• (Anti-HBs-Ab)

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HBeAg

• correlates with active viral replication
• Indicates high viral load and infectivity

36
CLINICAL COURSE

• Diagnosis detecting HBsAg and IgM core antibody
• ALT AST levels increase to between 500 to 5000
  U/L and fall after the acute phase
• Serum bilirubin level seldom increases above 10
  mg/dL
• Alkaline phosphatase and prothrombin time are
  usually normal or mildly elevated (1-3 seconds)

37
CLINICAL COURSE

• Chronic HBV
• Group 1
• evidence of active replication
• abnormal transaminases and
• higher viral loads
• Group 2
• nonreplicative state
• Decreased transaminases and
• Lower viral loads

38
Chronic HBV infection

• 10-fold increase in the risk of developing
  hepatocellular carcinoma (HCC)
• patients with both hepatitis B s Ag and HBe Ag,
  the risk increases to 60- fold
• HBV carriers, particularly those at highest risk
  (men over age 45, patients with cirrhosis, and
  those with a family history of liver cancer) -
  screened with ultrasound and alpha-fetoprotein
  for HCC, probably every 6 months

39
HBV THERAPY AND IMMUNIZATION

• Effective vaccines (90)
• Post-exposure prophylaxis-
• single dose of hepatitis B immune globulin
  (HBIG) injected intra-muscularly
• followed immediately by HBV vaccination
• 3 injections (10 µg of Engerix-B or 20 µg of
  Recombivax HB) intramuscularly in the deltoid
  muscle at 0, 1, and 6 months
• Smokers, the obese, or the elderly, or
  immunocompromised respond poorly

40
HBV Therapy

• Acute Supportive therapy only
• Require follow up to establish virus clearance
• Chronic
• suppress viral replication and prevent
  progression of liver disease
• compensated and decompensated cirrhosis and
  measurable HBV DNA

41
Chronic HBV Therapy

• Five agents
• I. Interferon alpha (side effects fatigue,
  muscle aches, fever, depression, and irritability
  / exacerbation of depression, psychosis, renal
  and cardiac failure, bacterial infections, and
  induction of autoimmunity )
• Peginterferon alfa 2a, at a dose of 180µg for 48
  weeks) in 2005 for treatment of patients with
  chronic hepatitis B

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Chronic HBV therapy

• nucleoside or nucleotide analogs
• 3 Lamivudine (1998)
• 4 Adefovir (2002)
• 5 Entecavir (2005)

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hepatitis

• Hepatitis C

44
HCV Distribution
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PREVALENCE

• 1 affected worldwide
• USA 3.0 million exposed (1.5 2.7 million have
  chronic hepatitis C infection)
• major route of infection was via blood
  transfusion
• (PCR) assays to screen pooled blood reduced the
  risk to less than 1/100000 units transfused

46
HCV infections

• most common route of transmission now is
  recreational intravenous drug use, which is
  responsible for perhaps as many as 50 of new
  infections
• having multiple sexual partners
• tattooing, body piercing and
• sharing straws during intranasal cocaine use

47
Other potential HCV infections

• Maternal-fetal transmission (10)
• HCV contaminated needle-stick injury (0-10)
• ? Screen previous drug users, HIV,
  hemophiliacs, hemodialysis, prior transplants and
  trnasfuses before 1992, needle stick, partners
  exposed

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Pathology of HCV

• the virus represents a "moving target" to the
  immune system
• Damage to the liver parenchyma is mediated by
  inflammatory cytokines
• various degrees of hepatic fibrosis
• progressive fibrosis and eventually cirrhosis
• Predictors of progression male sex, age at onset
  of infection, and the use of alcohol

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SIGNS AND SYMPTOMS

• very mild flu-like symptoms
• weight loss, fatigue, muscle or joint pain,
  irritability, nausea, malaise, anorexia and
  jaundice have been reported to rarely occur in
  the 2 to 26 week incubation period
• fatigue is probably the most frequent complaint
• depression, nausea, anorexia, abdominal
  discomfort, and difficulty with concentration

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Extra Hepatic Manifestations

• glomerulonephritis
• vasculitis
• pulmonary fibrosis

51
DIAGNOSIS

• ELISA HCV antibodies
• RIBA
• HCV RNA (PCR)
• Raised ALT
• Viral quantification
• Viral loads and genotype 1 are resistant to
  therapy (40 response) genotype 23 response
  rates 80

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THERAPY

• progress to chronic liver disease in up to 85 of
  patients
• interferon-based therapy given early in the
  course decreases the risk of progression to
  chronic infection
• Complete abstinence from alcohol
• Dietary supplements, herbs, and unconventional
  treatmentshave not been rigorously studied, and
  the results are extremely varied

53
Treatment Outcomes

• nonresponse
• Relapse and
• sustained virologic response (SVR) (undetectable
  virus in the serum 6 months after treatment )

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Individualized

• detectable HCV RNA
• elevated serum aminotransferase levels
• evidence of chronic hepatitis on liver biopsy
• absence of decompensation, and
• no contraindications
• combination alpha interferon and ribavirin
  therapy

• Specific contra-indications
• severe concurrent disease
• previous solid organ transplant
• autoimmune hepatitis
• Hyperthyroidism
• pregnancy
• or uncontrolled depression
• HIV decreased response rate (14-73 )

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Prognostics

• pre-treatment neuro-psychiatric assessment
• Psychosis and homicidal or suicidal ideation are
  strong contra-indications
• low pretreatment HCV RNA level, genotypes 2 or 3,
  female gender, low body mass index (BMI) and low
  hepatic iron load
• advanced liver disease or decompensated cirrhosis
  are also unlikely to respond, and frequently are
  unable to tolerate treatment

56
Therapy

• interferon alfa, as an immune modulator
• monotherapy (10 in genotype I and at best 30 in
  genotype 2 and 3)
• Side effects "flu-like symptoms", including
  fever, arthralgia, headache, depression,
  injection site inflammation and bone marrow
  suppression

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Therapy

• Combined Interferon Alfa Ribavarin (improved to
  around 40 (20 in genotype 1 and 65 in
  genotypes 2 and 3)
• Ribavirin contraindicated in patients with
  significant renal dysfunction (a creatinine
  clearance lt50 ml/min) and teratogenic
  (contra-indicated in pregnancy)
• fatigue in about 15 from a hemolytic anemia

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Sustained Viral Response Rate of HCV withDifferent Therapeutic Regimens Sustained Viral Response Rate of HCV withDifferent Therapeutic Regimens Sustained Viral Response Rate of HCV withDifferent Therapeutic Regimens Sustained Viral Response Rate of HCV withDifferent Therapeutic Regimens
  of Months SVR Genotype I SVR Genotype II or III
Interferon 6 10 20
INF/Riba 6 to 12 29 66
PegINF 6 to 12 20 40
PegINF/Riba 6 to 12 50 88
HCV Genotype I treated for 12 mo and Genotype 2 and 3 for 6 mo HCV Genotype I treated for 12 mo and Genotype 2 and 3 for 6 mo HCV Genotype I treated for 12 mo and Genotype 2 and 3 for 6 mo HCV Genotype I treated for 12 mo and Genotype 2 and 3 for 6 mo
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HCV Therapy

• monitored closely for complications or symptoms
  of the adverse reactions of combination therapy.
• evaluation for depression
• symptoms of irritability
• sleep disturbance
• visual disturbances
• as well as evidence of hyper- or hypothyroidism

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Complications

• most common indication for liver transplantation
  in the United States
• over the next twenty years, the proportion of
  infected patients with cirrhosis will increase
  from 16 to 32
• hepatic decompensation (up 106), hepatocellular
  carcinoma (up 81), and liver-related deaths (up
  180).

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HCV Recap

1. gt 60 become chronic HCV infection
2. cirrhosis -20 over a 20 year
3. Outcome affected by age at onset of infection,
   gender, co-infection with other viruses (HAV, HBV
   or HIV) or other medical conditions, as well as
   behaviors, such as alcohol consumption
4. Interferon-based treatment has a variable success
   rate in clearing the virus
5. risk of developing hepatocellular carcinoma (HCC)
   in chronic HCV 4 per year

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HCV Recap

• 7. screened at periodic intervals with ultrasound
  and alpha-fetoprotein
• 8. treatment with interferon has been associated
  with a lower rate of development of HCC

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Hepatology

• Cirrhosis

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features

• End result of injury that leads to both fibrosis
  and nodular regeneration.
• May be reversible if cause is removed.
• The clinical features result from hepatic cell
  dysfunction, portosystemic shunting, and portal
  hypertension.

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Cirrhosis

• Increased risk heavy alcohol use, obesity, iron
  overload
• Decreased risk higher coffee and tea consumption

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Diffuse nodularity
67
Symptoms and Signs
68
Stigmata of liver disease
69
Dupuytrens Contracture
70
Cirrhosis Ascites
71
TreatmentGENERAL MEASURES

• abstinence
• sodium restriction
• hepatic encephalopathy, protein intake should be
  reduced to 6080 g/d

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Complications

• Spontaneous bacterial peritonitis is heralded by
  abdominal pain, increasing ascites, fever, and
  progressive encephalopathy in a patient with
  cirrhotic ascites
• Cirrhotic ascites, dietary sodium intake may
  initially be restricted to 2000 mg/d
• Spironolactone (Aldactone ) AmilorideMidamor

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Ascites

• approach

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DEFINITION

• accumulation of fluid in the peritoneal cavity
• Clinically diagnosed only when 1.5 liter of fluid
  accumulates

75
Common Causes of Ascites
Extra-peritoneal Extra-peritoneal
Cirrhosis Cirrhosis
Congestive heart failure Congestive heart failure

Hypoalbuminemia Hypoalbuminemia
Nephrotic sydnrome
Malnutrition
Protein-losing enteropathy
Myxedema Myxedema
Pancreatitis Pancreatitis
Chylous ascites Chylous ascites
Peritoneal Peritoneal
Malignancy Malignancy
Ovarian cancer
Pancreatic cancer
Other
Infection Infection
Tuberculosis
Bacterial
Fungal
Parasitic
Endometriosis Endometriosis
76
risk factors for liver disease

• Especially
• alcohol consumption
• transfusions
• tattoos, injection drug use
• a history of viral hepatitis or jaundice
• and
• 5. birth in an area endemic for hepatitis

77
?tuberculous peritonitis

• immigrants, immune compromised hosts
• or
• severely malnourished alcoholics
• history of cancer or marked weight loss arouses
  suspicion of malignant ascites

78
Tuberculous Peritonitis (2)

• 70 HIV
• 20 non HIV
• At risk urban poor, patients with cirrhosis,
  and nursing home residents.
• low-grade fever, abdominal pain, anorexia, and
  weight loss
• ?CXR, PPD test
• ascites adenosine deaminase activity
• gt 30 IU/L
• laparoscopy establishes the diagnosis

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SIGNS OF LIVER DISEASE

• large abdominal wall veins
• FLOW CEPHALAD- PORTAL HTN
• FLOW DOWNWARDS- IVC OBSTN
• palmar erythema, cutaneous spider angiomas,
  gynecomastia, and Dupuytren's contracture.
  Asterixis
• left supraclavicular region or umbilicus
  LYMPHNODE

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Sister Mary Joseph Nodule

• Head Nurse to William Mayo
• Noticed that a firm, red, non-tender nodule in
  the umbilicus was often associated with advanced
  malignancy
• Results from spread of tumour within the
  falciform ligament
• 90 are adenocarcinomas
• Commonest primaries are stomach and ovary
• Primary tumour is almost invariably inoperable

81
CLINICAL ASCITES

• gt1500 ML OF FLUID
• ?OBESITY
• Lab workup
• serum-ascites albumin gradient (SAAG)
• subtract the ascitic fluid albumin from the serum
  albumin
• SAAG gt1.1 g/dL PORTAL HTN
• lt 1.1 g/dL NON-PORTAL HTN

82
IMAGING

• US
• CT
• LAPARASCOPY- USEFUL IN DETECTING PERITONEAL CAUSES

83
Porto Systemic Shunt

• Increased portal venous pressure (gt12 mm)
• Release of vasodilator (Nitric Oxide)
• generalized abdominal distention, flank fullness,
  and shifting dullness

84
Therapy

• minimization of intraperitoneal fluid
• decreasing abdominal discomfort and/or dyspnea
• minimizing consumption of alcohol, (NSAIDs), and
  dietary sodium

85

• NSAIDs inhibit the synthesis of renal
  prostaglandin and this can lead to
• renal vasoconstriction
• decreased diuretic response and
• acute renal failure

86
therapy

• Aggressive
• oral diuretics, therapeutic (or large-volume)-
• paracentesis
• transjugular intrahepatic portosystemic shunt
  (TIPS), and
• liver transplantation

87
Transvenous Intrahepatic Portal Shunt TIPS

• performed under conscious sedation
• by an interventional radiologist.
• The portal system is accessed through the jugular
  vein, and the operator inserts a self-expanding
  shunt between the portal (high-pressure) and
  hepatic (low-pressure) veins.
• The ultimate goal of the procedure is to lower
  portal pressures to lt12 mm Hg, the level at which
  ascites begins to accumulate

88
TIPS
89
OUTCOMES

• 50 survive 2 years
• refractory ascites-
• 50 death in 6 months and
• 75 in 1 year
• Liver transplants survive at least 2 years (85)

90
Hepatology

• Alcoholic Hepatitis

91
Forms of Alcoholic Liver Disease Forms of Alcoholic Liver Disease Forms of Alcoholic Liver Disease Forms of Alcoholic Liver Disease
   FattyLiver AlcoholicHepatitis Cirrhosis
Histologic specificity for alcoholic etiology No Yes No
Prognosis Excellent Variable Guarded
Reversible Yes Variable Generallyno
92
Risk of alcohol related liver disease

• Increases with the quantity and duration of
  alcohol intake
• Only one in five heavy drinkers will develop
  alcoholic hepatitis
• One in four develop cirrhosis

93
Risk of alcohol related liver disease

• Modest alcohol intake (up to 10 g/day) will also
  exhibit fatty changes
• More than 80 g/day in men and 20 g/day in women
  increases the risk of fatty liver
• Other causes for fatty liver obesity, insulin
  resistance, hyperlipidemia, malnutrition, and
  various medications

94
Risk of alcohol related liver disease

• daily alcohol intake of 40 grams
• More than 80 g/day increase in the severity of
  alcoholic hepatitis
• Daily intake in men/women gt60/20 significantly
  increases the risk of cirrhosis
• Steady daily drinking, as compared with binge
  drinking, appears to be more harmful

95
Alcohol Content of Some Common Beverages Alcohol Content of Some Common Beverages Alcohol Content of Some Common Beverages
Drink Amount (oz) AbsoluteAlcohol (g)
Beer 12 12
Wine 5 12
Liquor(80 proof) 1.5 12
96
PATHOPHYSIOLOGY

• Activates hepatic macrophages that then produce
  tumor necrosis factor-a
• This causes oxidative stress
• Oxidative stress promotes hepatocyte necrosis and
  apoptosis
• Exaggerated in the alcoholic who is deficient in
  antioxidants
• Causes inflammation and fibrosis
• Hypoxia induced by chronic alcohol use may
  contribute to hepatic damage

97
SIGNS AND SYMPTOMS

• Enlarged and smooth, but rarely tender, liver
• Alcoholic hepatitis anorexia and weight loss,
  abdominal pain and distention, or nausea and
  vomiting
• More severe and specific - encephalopathy and
  hepatic failure. hepatomegaly, jaundice, ascites,
  spider angiomas, fever

98
laboratory abnormalities

• Anemia, leukocytosis, and elevated
  aminotransferases
• Hyperbilirubinemia, prolonged prothrombin time,
  and depressed albumin
• Complications of portal hypertension such as
  variceal bleeding, ascites, or hepatic
  encephalopathy

99
DIAGNOSIS

• Ultrasonographic findings include a hyperechoic
  (bright) liver with or without hepatomegaly
• (ASTALT) is approximately 21 (does not exceed
  300 U/L)
• Require a more accurate estimation of alcohol
  intake

100
THERAPY

• Abstinence
• Referral to a chemical dependency team
• Nutrition (degree of malnutrition correlates
  directly with both short-term (1-month) 14 and
  long-term (1-year) mortality) 76

101
HEPATOLOGY
102
HEPATOLOGY

• GALLSTONES

103
GALLBLADDER DISEASE

• Usually asymptomatic
• Biliary colic
• intermittent
• severe pain in the epigastrium or
• right upper quadrant and at times
• between the scapula

104
GALLBLADDER DISEASE

• Obstruction of the cystic duct
• INFLAMED GALL BLADDER
• CHOLECYSTITIS-
• Inflammation infection

105
PREVALENCE

• 20.5 million
• 14.2 million women
• gt600,000 cholecystectomies per year
• 75 of Pima and other American Indian women over
  the age of 25 years have cholelithiasis
• Obesity and Pregnancy , HRT
• Diabetes
• Cirrhosis and hepatitis C - Males

106
PREVALENCE

• Drugs That increase the risk
• Clofibrate (Atromid-S )
• Octreotide (Sandostatin)
• Ceftriaxone (Rocephin)
• Drugs That decrease the risk Aspirin and
  NSAIDs

107
Reducing Factors

• Coffee appears to protect against gallstones in
  women
• High-fiber diet reduces the risk of
  cholecystectomy in women
• High intake of polyunsaturated and
  monounsaturated fats reduces the risk of
  gallstones in men

108
SIGNS AND SYMPTOMS

• Asymptomatic
• Right upper quadrant abdominal pain
• Nausea and vomiting
• Biliary colic
• Progress to cholecystitis (persistent pain and
  fever)
• Murphy's sign

109
DIAGNOSIS

• Right upper quadrant ultrasound
• Shows
• The presence of gallstones
• A thickened gallbladder wall and
• Pericholecystic fluid

110
THERAPY

• Cholecystectomy
• RED FLAG
• persistent right upper quadrant tenderness and
  
• develop fever or
• elevated white blood cell count
• Common bile duct stones (10) need to be removed
  separately

111
OUTCOMES

• Laparoscopic cholecystectomy procedure of
  choice
• Relief of pain (95)

112
Post-cholecystectomy Syndrome

• Small group of patients (mostly women)
• Biliary pain
• Conventional radiographic studies of the upper
  gastrointestinal tract and gallbladderincluding
  cholangiography
• Unremarkable
• Resected gallbladder shows chronic cholecystitis
  or microlithiasis

113
Postcholecystectomy Syndrome

• Continuing symptoms
• Right upper quadrant pain
• Flatulence and
• Fatty food intolerance
• DD Esophagitis / Pancreatitis / Radiculopathy
  / or Functional bowel disease

114
Postcholecystectomy Syndrome

• Rule out the possibility of choledocholithiasis
  or
• Common duct stricture as a cause of persistent
  symptoms
• Biliary pain associated with elevated liver tests
  and a dilated bile duct suggests sphincter of
  Oddi dysfunction or stenosis

115
Gallstones Chemistry

• Cholesterol (80)
• or
• Calcium bilirubinate (20)

116
Chemotherapy

• Cheno- and ursodeoxycholic acid
• Ursodeoxycholic Acid, UrsodiolActigall, Urso
• Most effective in patients with a functioning
  gallbladder and multiple small "floating"
  gallstones (15)

117
Acute Cholecystitis

• Steady, severe pain and tenderness in the right
  hypochondrium or epigastrium.
• Nausea and vomiting.
• Fever and leukocytosis
• Gallstone related (90)

118
Acute Cholecystitis

• Symptoms and Signs
• Precipitated by a large or fatty meal
• Sudden appearance of steady pain localized to the
  epigastrium or right hypochondrium
• Nausea and vomiting (75)
• Palpable gallbladder (15)
• Jaundice (25)

119
Lab Workup

• WBC- 12-15,000
• Bili 1-4 mg/dL
• ALT/AST- 300 IU
• AXR plain (15)
• US

120
Lab Workup

• The gallbladder contains both sludge and stones
• gallbladder wall thickening
• pericholecystic fluid and
• sonographic Murphy's sign

121
A Redflag

• Perforation
• Gangrene
• Sepsis
• Initially antibiotics therapy
• Folllowed by laparascopic removal

122
Choledocholithiasis
123
Choledocholithiasis

• CBD stones (15)
• Common in elderly

124
Lab Workup

• Acute AST/ALT elevation (1000 IU)
• Bili Elevation
• ALP Increase
• Amylase may be up if pancreatitis is present
• US/ ERCP/ Helical CT/ MRI

125
ERCP
126
(No Transcript)
127
DD

• Cancer of
• The pancreas
• Ampulla of Vater or
• Common duct
• Drug induced