38257492 jaundice master ppt
TRANSCRIPT
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Approach to the Patients with Jaundice
Dr Suresh Kubavat
MD (Internal Medicine)
Consultant Physician
Shradha Arogyamandir - Junagadh
9427257977
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Gross Hepatic Anatomy
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Gross Hepatic Anatomy
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Liver Histological Structure
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Liver Histological Structure
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Functions of the Liver1.Metabolism Fats ,Proteins,Carbohydrates,Hormones
2.Storage (as Glycogen)
3.Interconversion=Glucose-Fat-Amino acids
4.Production:Fatty acids,Triglycerides,Phos --pholipids,ketones,Cholesterol,Albumin,Fibrinogen
5.Exocrine:Bile-Bilirubin-Helps digestion
6.Detoxification of ciculating toxins.
7. Drug metabolism and excretion.
8. Removal of particulate matters-Kupffer
cells
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Normal Bile Physiology
300mg bile/day
2 roles: 1. excretion
2. emulsification of fat
Water (98%)
Bile Salts
Bile pigments (Bilirubin)
Fatty Acids
Lecithin (Fat emulsifier,Cell protector)
Cholesterol
Na,K,Ca,Cl,Hco3
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Normal Bilirubin Metabolism
Bile:300mg/Day-80% from aged dying RBCs
-20% from premature destruction in BM
HemoglobinHeme + GlobinHemeBiliverdin+CO+IronBiliverdin(Water insoluble)Binds with Albumin(becomes
water soluble)Liver:unconj bil taken up by hepatocytesconjugates to glucuronic acidBileexcr to intestinegoes to terminal ilium+colonbecomes unconjugatedconverted to urobilinogen80-90% excreted in faeces
as urobilins+10-20% absorbed thru intestineportal v.LiverReexcreted A small fraction esca es he atic u take excr in urine
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Pathophysiology Jaundice = Bilirubin staining of tissue @ level
greater than 3
Mechanisms:
production of bilirubin (Hemolysis)
hepatocyte transport
conjugation
Impaired excretion of bilirubin(Hepatitis,drugs,sepsis,
Dubin-Johnson )
Impaired delivery of bilirubin into intestine
surgically relevant jaundice orobstructive jaundice
Cholestasis refers to the latter two,
impaired excretion and obstructive jaundice
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Definition of Jaundice
Jaundice is yellow discoloration of the sclera,skin and mucous membranes resulting fromaccumulation of bilirubin.
Normal bilirubin levels are 0.4+0.2 mg per dl, with> 95% unconjugated.
Hyperbilirubinemia is separated into two classes :unconjugated (> 80% of total bilirubin) and
conjugated (>30 % of total bilirubin)
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Algorithm for PT with jaundice.History+Physical exam+Lab tests
Isolated elevation ofthe Bilirubin
Bilirubin & otherliver tests elevated
Directhyperbilirubinemia
Inherited disorders1. Dubin Johnson Syndrome2. Rotors Syndrome
Indirecthyperbilirubinemia
DrugsRifampicin
Hemolytic Disorders-Sphero,Ellipto,G6PD,Sickle,immuneIneffective erythropoiesis-Iron,Folate,B12 def,Thallesemia.
Inherited Disorders1. Gilberts Syndrome2. CriglerNajjar Syndromes
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ALGORITHM CONTINUED
Bilirubin & other liver tests elevated
Hepatocellular Pattern Cholestatic Pattern
SGPT/OT elevated out ofproportion to
Alkaline phosphatase
Alkaline phosphataseelevated out of proportion to
SGPT/OT
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Hepatocellular Pattern
1. Viral SerologiesHepatitis A IgMHepatitis B Surface Antigen
& core antibody (IgM)Hepatitis C RNA2. Toxicology screenAcetaminophen level3. Ceruloplasmin (If Pt < 40)4. ANA, SMA, LKM(Liver
Kidney MicrosomalAntibody), SPEP( Serumprotein electrophoresis)
Additional VirologicTesting
CMV DNA, EBV capsidantigen
Hepatitis D antibody(Ifindicated)
Hepatitis E IgM(Ifindicated)
If negative
If negative LiverBiopsy
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Cholestatic Pattern
UltrasoundDilated DuctsExtra hepaticcholestasis
CT/ERCP
Ducts not DilatedIntra hepaticcholestasis
Serologic testingAMAHepatitis SerologiesHepatitis ACMV, EBVReview Drugs
MRCP/Liver Biopsy
Liver Biopsy
Negative
AMA +ve
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Prehepatic
Unconguated Bil
LFTs N
Haptoglobins (aprotein in bloodthat combines withhb to form acomplex that isremoved from @ bythe liver)
Reticulocytes
Coombs test +ve
Urine urobilinogen +
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Hepatic ALT(SGPT)
ALP N or
Bil
Albumin
INR
Hepatitis serology
Autoantibodies
Anti-mitochondrial PBC
Anti-nuclear & antimicrosomal, Autoimmune
hepatitis
Caeruloplasmin
Wilsons
-Globulins
Cirrhosis esp autoimmune
Transferrin
Haemochromatosis
-foetoprotein, FP
HCC(Hepato cellula Carcinoma) in cirrhosis
H ti C
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Hepatic Causes Viral Hepatitis : A,B,C,D,E / EBV / CMV /Herpes Simplex.
Alcohol
Drug toxicity : Predictable: Paracetamol
Unpredictable:INH
Environmental toxins : Vinyl chloride (PVC)CaJamaica Bush Tea
Kava Kava
Wild mushrooms Wilsons disease
Autoimmune hepatitis.
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Alcoholic Liver Disease The history is the key 60 grams-aprox 60ml/day
Gynecomastia, parotids, Dupuytrens
Lab clues: SGOT/SGPT > 2, SGOT < 300
Alcoholic hepatitis:Anorexia, fever, jaundice,hepatomegaly
Treatment: Abstinence,Nutrition
Prednisolone (Antiinflamatory)
Pentoxifylline (Decreases the risk ofdeveloping hepatorenal syndrome andthus diminishes mortality.
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Alcoholic Liver Disease
Discriminant Function Formula:
DF =[4.6 x (Pt PT control PT)] + T.Bili
Consider treatment for DF > 32
Prednisolone 40 mg/day x 28 days
contraindications: infection, renal failure, GIB
Pentoxifylline 400 mg PO tid x 28days
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Autoimmune Hepatitis
Widely variable clinical presentations Asymptomatic LFT abnormality (ALT and AST)
Severe hepatitis with jaundice
Cirrhosis and complications of portal HTN
Often associated with other autoimmune dz
Diagnosis:
Compatible clinical presentation
ANA or ASMA with titer 1:80 or greater
IgG > 1.5 upper limits of normal
Liver biopsy: portal lymphocytes + plasma cells
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Acetaminophen Toxicity Safe Dose is < 4 gms/Day for an adult.
Danger dosages (70 kg patient)
Toxicity possible > 10 gm
Severe toxicity certain > 25 gm
Lower doses potentially hepatotoxic in:
Chronic alcoholics
Malnutrition or fasting
Dilantin, Tegretol, phenobarbital, INH, rifampin
-Antidote N acetyl cysteine within 16 Hrs
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Post - hepatic
ALT(SGPT) N or
ALP(Alk PO4)
Bil INR
CEA, Ca19.9
Pancreatic &cholangio Ca
Ch l t ti J di I t h ti
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Cholestatic Jaundice-Intrahepatic
Viral : B & C
Fibrosing cholestatic
HepA,EBV,CMV
Alcoholic hepatitis
Drug Toxicity :
Pure cholestasis-Anabolic Steroids
Contraceptives
Cholestatic Hepatitis
Chlorpromazine
Erythromycin
Chronic cholestasis
Chlorpromazine,
Prochlorperzine.
Primary Biliary Cirrhosis
Prim Scler Cholangitis
Vanishing Bile duct Syn
Inherited progr familialintrahepatic cholestasis
Benign recur cholestas
Cholestasis of Preg
TPN
Non hepatobil sepsis
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Cholestatic Jaundice-Intrahepatic- cont
Benign Post op cholest
Paraneoplastic Syndr
Venoocclusive Dis
Infiltrative diseases
TB,Lymphoma,sarcoid
Ch l t ti J di E t h ti
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Cholestatic Jaundice-Extrahepatic A. Malignant
Cholangiocarcinoma,Pancreatic ca, Ca-GB,
Ampulla Ca, Malig involvement of porta hepatis
lymph nodes.
B. Benign
Choledocolithiasis,Post op biliary stricture,
Primary sclerosing cholangitis, Chronic
pancreatitis, AIDS Cholangiopathy,
Mirizzi Syndrome:stricture of common hepatic duct
Parasitic disease- Ascariasis.
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Obstructive JaundiceCBD stones (choledocholithiasis) vs. tumor
Clinical features favoring CBD stones: Age < 45
Biliary colic
Fever Transient spike in AST or amylase
Clinical features favoring cancer:
Painless jaundice
Weight loss
Palpable gallbladder
Bilirubin > 10
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Ascending Cholangitis
Pus under pressure Charcots triad: fever, jaundice, RUQ pain
All 3 present in 70% of patients, but fever > 95%
May also present as confusion or hypotension
Most frequent causative organisms:
E. Coli, Klebsiella, Enterobacter, Enterococcus
anaerobes are rare and usually post-surgical
Treatment:
Antibiotics: Levaquin, Zosyn, meropenem
ERCP with biliary drainage
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Ascending CholangitisIndications for Urgent ERCP
Persistent abdominal pain
Hypotension despite adequate
IVF Fever > 102
Mental confusion Failure to improve after 12 hours
of antibiotics and supportive care
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Obstructive JaundiceMalignant Causes
Cancer of the Pancreas
Cancer of the Bile Ducts(Cholangiocarcinoma)
Ampullary Tumors
Portal Lymphadenopathy
P i Bili Ci h i
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Primary Biliary Cirrhosis Cholestatic liver disease (ALP)
Most common symptoms: pruritus andfatigue
Many patients asx, and dx by abnormal LFT
Female:male ratio 9:1
Diagnosis:
Compatible clinical presentation
AMA titer 1:80 or greater (95% sens/spec) IgM > 1.5 upper limits of normal
Liver biopsy: bile duct destruction
Treatment: Ursodeoxycholic acid 15 mg/kg
Primary Sclerosing Cholangitis
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Primary Sclerosing Cholangitis Cholestatic liver disease (ALP)
Inflammation of large bile ducts 90% associated with IBD
but only 5% of IBD patients get PSC
Diagnosis: ERCP (now MRCP)
No autoantibodies, no elevated globulins
Biopsy: concentric fibrosis around bile ducts Cholangiocarcinoma: 10-15% lifetime risk
Treatment: Liver Transplantation
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Diagnosis ofImmune-Mediated Liver Disease
LFT Serology QuantitativeImmunoglobulins
Biopsy
AIH SGPT ANA
ASMA
IgG Portalinflammation
Plasmacytes
Piecemealnecrosis
PBC ALP AMA IgMBile duct
destruction
granulomas
PSC ALP none normalPeriductalconcentric
fibrosis
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Common causes of Jaundice
Hepatitis
Obstructive jaundice
Primary liver cancer
Liver secondaries
Cirrhosis
Haemolysis
Gilberts syndrome
Septicaemia
U l C f J di
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Unusual Causes of Jaundice
Ischemic hepatitis
Congestive hepatopathy
Wilsons disease
AIDS cholangiopathy
Amanita phalloides (mushrooms)
Jamaican bush tea
Infiltrative diseases of the liver
Amyloidosis
Sarcoidosis
Malignancy: lymphoma, metastatic dz
Wilsons Disease
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Wilson s Disease Autosomal recessive copper metabolism
Chronic hepatitis or fulminant hepatitis Associated clinical features:
Neuropsychiatric disease
Hemolytic anemia
Physical exam: Kayser-Fleischer rings
Diagnosis: ceruloplasmin, urinary Cu Treatment: d-penicillamine
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LFTs and urine summary
Blood Urine
SGPT ALP Bil Urobilinogen Bilirubin
Pre-hepatic
N N Present absent
Hepatic N or N Present
Post-hepatic
N or absent Present
B d Diff i l Di i
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Broad Differential Diagnosisproduction transport or
conjugation
Impaired
excretion
Biliary
obstruction Unconjugate Unconjugate Conjugated Conjugated
Hemolysis Gilberts Rotors CH/CBD stone
Transfusions Crigler-Najarr DubinJohnson Stricture
Txfusion rxn Neonatal Cancer Cancer
Sepsis Cirrhosis Cirrhosis Chronic
pancreatitisBurns Hepatitis Hepatitis PSC
Hgb-opathies Drug inhibition Amyloidosis
Pregnancy
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Causes of JaundiceUnconjugated hyperbilirubinemia
Hemolysis
Glucose-6-phosphate deficiency Medications
Bilirubin overproduction Ineffective erythropoiesis Large hematoma Pulmonary embolism with infarction
Neonatal causes Physiologic jaundice Breast milk jaundice
Uridine diphosphate glucuronosyltransferase deficiencies Gillberts syndrome Crigler-Najjar syndrome ( I and II)
Miscellaneous causes Hypothyroidism Thyrotoxicosis Fasting
Causes of Jaundice
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Causes of JaundiceConjugated hyperbilirubinemia
Congenital causes Rotors syndrome
Dubin-Johnson syndrome Choledochal cysts
Familial disorders Benign recurrent intrahepatic cholestasis Cholestasis of pregnancy
Hepatocellular defects
Ethanol abuse Viral infection
Cholestatic syndromes Primary billiary cirrhosis Primary sclerosing cholangitis Billiary obstruction
Pancreatic disease Systemic disease
Infiltrative disorders
Postoperative complications
Renal disease
Sepsis
Medications
History
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History
Oral Exposure:Alcohol,Chemicals,Rx Med,OTC Med,Complementary med,Alternative Med,Contamin food.
Parenteral Exposure:IV inj,Transfusions,
Tattoo(Hep C), Intranasal drugs(Hep C)
Sexual exposure(Hep B).
Exposure to Endemic area-Travel history(Hep A).
Professional Exposure:Drs,Paramedics(Hep B+C).
Occupational exposure to Hepatotoxins.
Hepatotoxins
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Hepatotoxins
Molibdinum
Nickel.
Phosphorus.
Selenium.
Thallium.
Tin.
Antimony
Arsenic
Barium
Bismuth.
Cadmium.
Chromium.
Copper.
Iron. Lead.
Manganese.
Occupational Exposure
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Occupational ExposureOccupation Maker Worker User
Artificial pearls
Air Pilots, Hanger workers
Cement,Rubber,Plastic,Leather
Chemical,Pharma industry
Color,Dye,Insecticides
Glass,Ink,Paint,Perfumes
Dry cleaners,Varnish,Waterproofer
Metal polish
Refrigeration,Printers
Soap,Thermometer,Wax
Tobacco denicotisers.
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History for the Jaundice Patients
Related to viral hepatitis Preceding arthralgia/myalgia
Blood transfusions B
Intravenous drug use B
Needle stick exposure B
Sexual practices HIV hepatitis
Contact with jaundiced persons B
Work in renal dialysis units B
Surgeons in trauma units - B
exposed to IV drug users - B
Shared razors/tooth brushes - B
Body piercing (ears,nose) -B
Tattoos -B
SYMPTOMS
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SYMPTOMS
Fever- Low gr to High grade
Low gr-hepatits
High gr + RUQ abd pain-Choledocolithiasis,Ascending colangitis.
Arthralgia,Myalgia Rash
Anorexia, Wt loss
Avulsion to tobacco Abd Pain-Mild/Severe, Acute/Chronic
Pruritus
Change in urine,stool colour
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Physical Examination
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y
Ascites+Jaundice.
Laennecs(Alcohol
ic)+other cirrhosis
Cirrhosis
Malignancy
Abd.Malignancy
Murphys sign :Severe RUQ tenderness
with resp arrest in inspiration.
Enlarged tender liver,
Jugular venous distention, edema, Enlargedtender liver.
Enl supracl node(Virchows node),Periumbilical
node(sister marryjosephs node),Nodular hard liver.
Spider nevi,palmar erythema,gynecomastia,caputmedusae,Dupuytrens contracture,Enlaged parotids,testicular
atrophy,R.pl effusion,Enlarged L.lobe of liver,Ascites,Enl spleen
.
CholecystitisAcute Cholangitis
ViralHepatitis,Amyloidosis,
R.Heart failure.
R.Sided Heartfailure
Spider Nevi
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Spider Nevi
Palmar Erythema
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Palmar Erythema
Gynecomastia
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Gynecomastia
Caput Medusae
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Caput Medusae
Dupuytrens contracture
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Dupuytren s contracture
Virchows Node
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Virchow s Node
Sister Marry Josephs Nodule.
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y p
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Gross specimen of cirrhosis
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pof the liver
Evaluation of the Jaundiced Patient
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PHYSICAL EXAM
BP/HR/Temp
Mental status
Asterixis
Abd tenderness
Liver size
Splenomegaly
Ascites
Edema
Spider angiomata
Hyperpigmentation
Kayser-Fleischerrings
Xanthomas
Gynecomastia
Left supraclavicularadenopathy(Virchows node)
Common causes of Jaundice and
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Common causes of Jaundice andrelevant investigations
Acute hepatitis Hepatitis serology
HBsAg, IgM anti-HBc, HBeAg, Anti-HBe
IgM anti HAV, Anti Delta antibody
Anti HCV Ig M anti HEV
IgM EBV, IgM CMV, IgM Lepto antibody
Pancreatic/biliary disease
Ultrasonography
Endoscopic retrograde cholangio-pancreatography
Percutaneous transhepatic cholangiography
CT Scanning
MRI-MRCP
Common causes of Jaundice and
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Common causes of Jaundice andrelevant investigations - contd
Malignancy Liver biopsy
Alpha fetoprotein
Cirrhosis
Liver biopsy Immunoglobulins
Auto antibodies
Iron studies
Serum, urine and liver copper; serum ceruloplasmin Alpha 1 antitrypsin
Common causes of Jaundice and
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Common causes of Jaundice andrelevant investigations - contd
Haemolysis
Reticulocyte count
Haptoglobin
Direct and indirect Coombs Test
G-6-P-D level
Gilberts Syndrome
Increase in unconjugated bilirubin following 2-3days on 1 400 calorie diet
Tips on Interpretation of Lab Tests
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p p SGPT?OT > ALPHepatocellular Process ALP > SGPT/ OTCholestatic Process Bilirubin : Increased in both but if
D>I : Cholestatic
I>D : Prehepatic.
D=I : Hepatocellular
.Albumin if normal Acute cause likeHepatits,Choledocolithiasis.
Prothrombin time: chronic cause + Signific hepatocelldysfunction.
If PT improves after inj Vit K Good liver functions.If PT doesnt im rove afterKSev he atocellular in ur .
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Haemolytic anaemia
Mechanism Examples
Abnormal red cell Hereditary spherocytosismembrane Drug e.g. Sulphonamides
sulphonylureas, alpha-
methyldopa, levodopaPrimary immunedeficiency
Rigid red cell membrane Sickle cell , Thalassaemia
Trauma to red cells Cardiac haemolysis (prostheticvalves) Microangiopathichaemolysis
Commonly used drugs causing jaundice
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Commonly used drugs causing jaundice
Drugs causing hepatitis
Amitriptyline Isoniazid
Erythromycin (estolate)
Nitrofurantoin
Paracetamol (more than 4g a day)
Ferrous sulphate overdose
Halothane
Drugs causing cholestasis
Oral contraceptives
Chlorpromazine Haloperidol
Chlorpropamide
Causes of postoperative jaundice
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Causes of postoperative jaundice Hypertension/cardiac failure
Post-transfusion hepatitis Drugs including anaesthetics, particularly halothane
on second exposure
Unmasked chronic liver disease
Unmasked biliary tract disease
Pulmonary embolism
Acalculus/acute cholecystitis
Transfusion load/haemolysis post cardiopulmonarybypass pump
Cholestasis following major abdominal surgery &TPN
Sepsis (pneumonia,urinary tract infection)
Liver biopsy indications
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Liver biopsy- indications Assessment of abnormal liver function tests
Diagnosis and prognosis of chronic hepatitis and/or cirrhosis
Confirmation and prognosis of alcoholic liver disease
Detection of systemic disorders involving the liver, including fever ofunknown origin
Assessment and severity of drug inducted liver injury
Confirmation of suspected hepatic malignancy, primary or metastatic
Confirmation of multisystem infiltrative disorders
Screening of relatives of patients with familial disease
Tissue of culture
Evaluation of response to therapies for liver disease (e.g. Wilsonsdisease, hemochromatosis, autoimmune hepatitis, chronic viral hepatitis)
Exclusion of graft rejection, reinfection, or ischemia after liver transplant
Li bi t i di ti
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Liver biopsy- contra-indications
Absolute Relative
Severe coagulopathy Ascites
PT > 3 seconds prolonged
Platelets < 60 000/mm
Abnormal bleeding time
Suspected echinococcal disease
Presumed hemangioma
Uncooperative patient
Critical Questions in the Evaluation
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Critical Questions in the Evaluationof the Jaundiced Patient
Acute vs. Chronic Liver Disease
Hepatocellular vs. Cholestatic
Biliary Obstruction vs. Intrahepatic Cholestasis
Fever
Could the patient have ascending cholangitis?
Encephalopathy
Could the patient have fulminant hepatic failure?
Evaluation of the Jaundiced PatientLAB EVALUATION
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LAB EVALUATION
AST-ALT-ALP
Bilirubintotal/indirect
Albumin
INR
Glucose
Na-K-PO4, acid-base
Acetaminophen level
CBC/ lt
Ammonia
Viral serologies
ANA-ASMA-AMA
Quantitative Ig
Ceruloplasmin
Iron profile
Blood cultures
D i hi h SGPT/OT
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Drugs causing high SGPT/OT
Aspirin,PCM
Brufen,Naproxen
Phenytoin,Sod
valproate
Carbamazepine
Tetra,Sulpha,TMP
INH,NFT,Fluconaz
Statins
Niacin
Amiodarone
Hydralazine
Quinidine
Tricyclic Antidep
Oth di i b OT/PT
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Other disease causing abn OT/PT
Hemachromatosis
Wilsons disease
Alpha 1 antitrypsin def(with emphysema)
Celiac sprue
Crohns disease
Ulcerative colitis
Evaluation of the Jaundiced Patient
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Evaluation of the Jaundiced Patient
Ultrasound:
More sensitive than CT for gallbladder stones Equally sensitive for dilated ducts
Portable, cheap, no radiation, no IV contrast
CT:
Better imaging of the pancreas and abdomen
MRCP:
Imaging of biliary tree comparable to ERCP
ERCP:
Therapeutic intervention for stones
Brushing and biopsy for malignancy
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Utility of Liver Function Test
Sensitive and non invasive method of screening forthe presence of liver dysfunction
The pattern of test abnormalities may allow to
recognize type of liver disorder
To assess the severity of liver disorder
To follow the course of disease
THANK YOU ALL !
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THANK YOU ALL !
Thanks to my sonVishwas
for helping me inpreparing this PPT
presentation !