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Payawal
Kupffer Cells
-sinusoids, cells , FIXED MACROPHAGE, removes alcohol etc..
ITO cells
-fat/lipid storring cells
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Liver, Pancreas & Gall Bladder Dr. Payawal
-stellate cells
-store retinoic acid(vit a)= tx of pimples LABORATORY TEST
-normally is quiet, quiescence
-always activated in liver disease I.Transaminases
st
-if activated, in a liver disease, releases collagen, 1 step
towards cirrhosis, so if SGPT is elevated, stellate cells are 1.SGPT / ALT
activated. -search enzyme / tracing enzyme
-modified fibroblast, revert to type strategy, or quiescence -found at zone 1 ( peri-portal zone ) :so oxygenated
-half life is 48 hrs.
*breakdown of hepatocytes,stimulated by the TGF- -released by the hepatocytes into the liver as it is injured
alpha(autocrine factor made in the hepato cells) ang -found int the cyrosol of the liver
HGF(hepatocyte growth factor) by fat storage cells and tumor -only seen in the liver
cells -slight elevation is needed attention, something happening to
the liver
st
*Hepatocytes-able to regenerate back -1 enzyme released in liver damage
-inflammation of the liver
*Transformation of the fat storing cells into fibrocytes is -liver is normal even elevated
released by the Kupher cells
2.SGOT / AST
*repeated damage = fibrosis -found both in the cytosol and mitochondria
-mitochondria is the oxygen bearing in the cell
if affected means Necrosis
-abundant in other organs like Heart, skelatal muscles and
blood
eq. Hazing : release sgot from muscles
st
Summary of the 1 lec: if high, look for PASA
Major functions of the Liver -if SGOT is higer than the SGPT = Necrosis than inflammation
excretion of bilirubin === liver disease of the patient
synthesis of plasma proteins : Albumin is in worst setting
synthesis of Vit K dependent clotting factors like
2,7,9,10 2 questions: / 2 conditions Sgot>Sgpt :
1.Is this a bad liver
Minor functions: 2.Is the patient dringking alcohol
bile production
porphyrin metabolism -increased in heart attacts, jogs a lot, exercise, muscle
-colored pigment (yellowing ) building
stores vitamins ang sugars
glucose metabolism: gluco............ -will only tell the kind of activity your liver has
HY's Law:
in taking drugs and SGPT increases, correlate it with your
HISTORY AND P.E. Total Bilirubiin, and log it together:
1.if SGOT is high but there is no jaundice, no elavation of
I.High Risk Behavior Bilirubin = Temple's Corollary
-risk for IV drugs 2.SGPT is elevated and Increased Bilirubin = Impending Liver
-multiple sexual partners failure ( problematic )
-tatoo : needles and solutions are not changed
: Hepa C (not B ) II.BILIRUBIN
-vertical transmission -degradation of heme and globin
-non sterile body piercing -heme is excreted predominantly via the bile
-alocohol abuse -to liver, to intestines, to urine
ALP
-immunolocalized microvilli in the bile
-the only test to asssess inflammation of the Bile
-non-hepatic in origin, incresed in cholestasis, causing
obstruction of the billiary tract
LIVER
1.5 kg, wedge shape
4 lobes right, left, caudate, quadrate
Double blood supply
o Hepatic artery 20% of blood flow is 02
rich Diagrammatic representations of the morphologic features of
o Portal vein 80%, nutrient rich acute and chronic hepatitis. Bridging necrosis may also occur
Hepatic arteries in acute hepatitis.
Portal- Venous blood
Acini/ portal triad ACUTE HEPATITIS
Lobules- Central vein Swelling and Apoptosis
Piecemeal or bridging, panacinar necrosis
Inflammation- Lymphocytes, Macrophages
Ground glass hepatocytes HBV
Mild fatty change HCV
Portal inflammation and Cholestasis
FULMINANT HEPATITIS
*Zone 1 is adjacent to the portal triad. Hepatic failure within 2-3 weeks
Reactivation of chronic or acute hepatitis
Liver function Massive necrosis, shrinkage, wrinkled
Metabolism- Carbohydrate, Fats and Protein Collapsed reticulin network
Secretory- Bile, Bile acids, salts and pigments Only portal tracts visible
Excretory- bilirubin, drugs, toxins Little or massive inflammation time
Synthesis- albumin, coagulation factors More than a week regenerative activity
Detoxification- toxins, ammonia, etc
CHRONIC HEPATITIS
JAUNDICE Persistent and active types (CPH/CAH)
Yellowish discoloration of skin and sclera due to Lymphoid aggregates
excess serum bilirubin > 40umol/l(3mg/dl) Periportal fibrosis
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Liver, Pancreas & Gall Bladder Dr. Payawal
Necrosis with fibrosis bridging fibrosis o Conjugated/ direct bilirubin, high colored
Cirrhosis regenerating nodules urine
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Liver, Pancreas & Gall Bladder Dr. Payawal
o Oral cholecystography:
Biliary contrast medium
A fatty meal- to contract the bile
duct
o Intravenous cholangiography
o Percutaneous transhepatic cholangiography
(PTC)
Show intra and extra hepatic
biliary duct clearly
Complication: bile leakage
o Cholangitis
Gallbladder: body, fundus, neck
o Hemorrhage
Level of the Stones: o Endoscopic retrograde
Gallbladder-dyspeptic symptoms cholangiopancreatography
Cyst duct-acute cholecystitis Outline the biliary tree and
Common bile (not fully obstructed) -dyspepesia or pancreatic duct
abdominal pain Inspect the biliary tree and
pancreatic duct
The level of the symptoms depend where the stone is located Inspect the ampulla of vater
*Common bile duct theory: the pancreatic duct and the Exam of fluid of duodenum, bile,
common bile duct joins together to form single opening
pancreatic fluid
Carlot triangle:
The triangle bounded by the common hepatic duct o Endoscopic sphincterotomy (EST)
medially, the cystic duct inferiorly and the inferior o Endoscopic naso-biliary drainage (ENBD)
surface of the liver superiorly is known as calot o Computed tomography (CT)
triangle. o Magnetic resonance
The fact that cystic artery, right hepatic artery and cholangiopancreatography (MRCP)
para-right hepatic duct run within the triangle makes o Cholangiopancreatography during
an important area of dissection during operation
cholecystectomy. o Percutaneous transhepatic cholangiography
Anatomy Cholelithiasis
The sphincter of Oddi: Including: gallstones and biliary duct stones
In China:
o The proximal bile and pancreatic ducts and
Before 1981
the common channel are surrounded by Gallstones < biliary duct stones
circular and longitudinal smooth muscle, Cholesterol stones < pigment stones
this muscle complex is known as the Now
sphincter of Oddi. Gallstones >biliary duct stones
Cholesterol stones > pigment stones
*a sphincter dysfunction can cause an additional pin to the
patient Classification of stones
1. Cholesterol stones: yellow stones, hard, layed on
Special investigation of the biliary tract cross-section, usully caused by infections
Ultrasound 2. Pigment stones: crumble when squashed
Non-invasive, painless, easily performed 3. Mixed stones: radio-opaque
First choice for biliary tract disease 4. Black stones
Bile duct stones: *left hepatic duct=more pigment stones
Stones in gallbladder:
High echo which cast an acoustic shadow and which LOCALIZATION OF STONES
move with changes in posture SITE TYPE PERCENT
Jaundice differential diagnosis: Gallstones Cholesterol stones or
mixed stones 50%
Dialation of the ducts distl part
(cholesterol mainly)
CBD: diameter>1.0cm
Extra hepatic bile Primary stones: pigment
Other disease: cholecystitis, tumor etc. duct stones stones and mixed stones
During surgery: to detect bile duct stones (bile pigment mainly)
20-30%
secondary stones:
*sensitivity-the disease is there you can see it cholesterol stones (from
*specificity-the disease is not there, cannot be seen gallbladder)
Radiology Intra hepatic bile Primary bile duct
o Plain abdominal radiograph: duct stones (left > stones: pigment stones
20-30%
Radio-opaque gallstones right) and mixed stones (bile
Air in the biliary tree pigment mainly)
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Liver, Pancreas & Gall Bladder Dr. Payawal
Pigment stones:- due to infection -anatomy variation: cyst duct runs parallel
form of calcium bilirubunate to the hepatic duct
bilirubin conjugated with glucuronide B-
glucoronidase produced by E. coli can split the molecule Mucoceole of the gallbladder:
unconjugated bilirubin precipitates as salt. -a stone impacts in the cystic duct without
bacterial infection
Gallstones ( cholecystolithiasis)
Risk factor: -bile reabsorbed
Women are three times more likely than men to
develop stones -the epithelium continues to secrete
Obesity mucous, which is called white bile
Pregnancy
Dietary factors: high energy, low in fiber Stones migrate though the cystic duct into the
Fasting common bile duct: infection, jaundice
Biliary infection Impaction of a small stone at the ampulla of Vater
Parasitic infestation and occlusion of the pancreatic duct causes
Deaibetes mellitus pancreatitis
TPN
Gastric surgery o Painjaundicefever= charcots triad, obstruction
Cirrhosis of liver of common bile duct
Chronic haemolyticanaemia o Feverpainjaundice= viral hepatitis/ infection
o Jaundicefeverpain= pancreatic cancer
Sign
Right upper area of the abdomen tenderness,
rigidity, rebound tenderness
Gallbladder palpable
Murphy sign: inspiratory arrest during subcostal
palpation
Jaundice: common bile duct stones or Mirizzi
syndrome
Fever and chill with infection
Treatment
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Liver, Pancreas & Gall Bladder Dr. Payawal
Ranson Criteria
Admission
o Age > 55
o WBC > 16, 000
o Glucose > 200
o LDH > 350
o AST >250
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