liver disease chapter8

8/2/2019 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!

liver disease chapter8

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