Download - Liver Disease Chapter8
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"With ordinary talent and
extraordinary perseverance, all
things are attainable."- Thomas E. Buxton
"Achievement is connected
with action, not in genes..!- Conrad Hilton
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CLINICAL BIOCHEMISTRYII (SBD 0113)
MISS SUZAILA BT.ARSAD
LIVERDYSFUNCTION
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Liver Functions:
Metabolism Carbohydrate, Fat & Protein
Secretory bile, Bile acids, salts & pigments
Excretory Bilirubin, drugs, toxins
Synthesis Albumin, coagulation factors
Storage Vitamins, carbohydrates etc.
Detoxification toxins, ammonia, etc.
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FUNCTION OF LIVER
Making bile to help digest foods
Bile acid synthesis & secretion
Stopping cuts from bleeding (coagulation)
Responsible for the synthesis of prothrombin, factor VII, IX,and X from vitamin K absorption.
Filtering toxic chemicals from the body
Remove waste products of nutrient breakdown
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Helps with disposing of bilirubin excretes bilirubin into the small bowel so that bowel bacteria can change it into the
safe green colored biliverdin.
Helping to build muscles/ proteins
Plasma protein synthesis Lipid & lipoprotein synthesis
Glucose homeostasis
Albumin is synthesized exclusively in the liver albumin is essential for carrying molecules (and drugs), and for keeping fluid in the blood
vessels.
Hypoalbuminemia causes fluid shift into tissue and patient will show signs of edema.
albumin decreases in malabsorption & tumor necrosis, or any form of chronic liver disease.
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Role of the liver (cont)
Storing energy
Store vitamins A, D, E and K, & B12
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Liver blood supply
Blood entersthe liver from
the hepatic artery and theportal vein and leavestheliver from the hepatic vein.
The blood from the artery
carries oxygen while the
portal vein carries nutrients
from the intestine.
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Liver regeneration
If individual hepatocytes are destroyed but thearchitecture of the lobule is not destroyed, theremaining hepatocytes will totally regenerate theliver parenchyma.
If whole lobules are destroyed, the remaininglobules will expand. They will function normally,though bile may not be drained quite so well.
Of course, if scar tissue alters the flow of bloodthrough the liver (i.e., cirrhosis has occurred),regeneration will only produce less-than-fully-perfused nodules of liver cells.
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Hepatic failure biochemicalchanges
Electrolyte imbalance Eg. Na and Cl fall
Severe metabolic acid-base imbalance
Hyperglycaemia
Renal failure exposure of glomeruli to toxin
Increaseblood NH3 failed to detoxify
Hypoalbuminemia - Edema/ascites
Hemorrhage
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Ascites
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Alcoholic Fatty Liver
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Alcoholic HepatitisDiagnostic Studies
A. Laboratory Test:
The SGOT (AST) 2-10xs normal
SGPT (ALT) is less elevated
Bilirubin mild to moderate
Alk phos is usually 2-3xs normal
Globulins elevated with reverse A/G ratio
Prothrombin time elevated (poor prognosis)
Leukocytosis
Blood NH3 (Ammonia) level
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Other causes ofChronic Hepatitis
Inherited Chronic Liver Disorders
A. Wilsons disease
B. Hemachromatosis
C. Alpha 1-antitrypsin deficiency
D. Reye syndrome
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Wilsons disease
genetic disorder of copper metabolism.
abnormal accumulation of copper in thehepatocytes.
The defect is in the ceruloplasm which carries thecopper.
Haemachromatosis
A group of disorders with excessive absorption ofiron.
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Primary cause unknown
Secondary- Iron overload :
anemias
cirrhosis
Dietary
Diagnosis:
Lethargy, weakness in men40-60 yo
Skin hyperpigmentation
Diabetes 30-60% of pts
arthopathy
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Alpha 1-Antitrypsin DeficiencyAlpha 1-antitrypsin is potent protease inhibitor found in the serum,
body fluids, & tissues
It is synthesized by the liver to protect from tissue injury resultingfrom protease like trypsin
Reyes syndrom only happens in kids less than 15 years old.
The cause is unknown, but it is strongly associated with Aspirin useduring flu's (fever).
Symptoms: Nausea, vomiting, hyperactivity, confusion, seizures, &coma, Increasing drowsiness,
fatty infiltration
Chemistry: elevated liver enzymes, NH3
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CIRRHOSIS
Terminal stage of chronic liver damage
Most common cause:
Chronic excess alcohol ingestion Hepatitis -particularly Hep B
Autoimmune ds
Difficult in coping with food,esp fatty meals
Reduced capacity to metabolize drugs
Itch
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Fibrotic bands ofconnective tissue
change the structure
of the liver
Inflammation causesdegeneration anddestruction of liver
cells
Tissue becomesnodular
Nodules block bileducts and normalblood flow
throughout the liver
Blood flow changesoccur fromcompression by the
fibrous tissue
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Pathogenesis:
Hepatocyte injury leading to necrosis. Alcohol, virus, drugs, toxins, genetic etc..
Chronic inflammation - (hepatitis).
Bridging fibrosis.
Regeneration of remaining hepatocytes
Proliferate as round nodules.
Loss of vascular arrangement results inregenerating hepatocytes ineffective.
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Cirrhosis
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Cirrhosis
Fibrosis
Regenerating Nodule
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Ascitis in Cirrhosis
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Micronodular cirrhosis:
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Liver Biopsy Cirrhosis
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Cirrhosis
ClinicalFeatures
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Signs of liver ds and causes
Jaundice- diminished bilirubin secretion
Fetor hepaticus- sulfur compounds produced byintestinal bacteria, not cleared by liver
Spider angiomas, palmar erythema, & gynecomastia-elevated estrogen levels
Ecchymoses- decreased synthesis of clotting factors
Xanthomas- elevated cholesterol levels
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Hypoglycemia- decreased glycogen stores
Hypersplenism- portal hypertension
Encephalopathy, asterixis- portosystemic shunt,NH3
Hepatorenal syndrome (rapid decline of GFR)-
renal failure of unknown pathogenesis, kidneysare normal (may be transplanted), assoc cascites, almost always fatal
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Learn from the
mistakes of others.You can't live long
enough to make them
all yourself!