Evaluating Liver Disease and Dysfunction

8/6/2019 Evaluating Liver Disease and Dysfunction

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AbaxisUniversityEvaluatingforLiverDamageandDysfunction

AndrewJRosenfeld,DVMABVP


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SectionI: PreCaseandCaseWorksheet


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Instructions: Prior to taking theonlinecourse,please review thecoursenotes

andevaluatethehospitalcase. Pleasetakesometimeandfillouttheprecourse

sectionof thecase to thebestofyourability. Once in lecture, thecasewillbe

discussed and new diagnostic testing and treatment options will become

available. As the class progresses, each team member will outline diagnostic

testing and treatment concerns to help identify the primary and secondary

concerns of the patient, understand treatment options and be able to discuss

theseconcernswiththeclient. Goodluck.

PrecourseSectionPleasefilloutpriortoattendingtheonlineclassroom

Signalment: Pewter,20kgMaleNeutered

5yearoldEnglishbulldog

CC: Lethargic,depressed,anorexicandhavingsoft

stoolfor7days.

InitialTriageExamination

Temp: 101.2degreesFahrenheit Pulse: 160 Resp:5060breaths/min CRT: 2 secs

AbaxisUniversityCaseWorkSheet

EvaluatingforLiverDamageandDysfunction

A.Rosenfeld,DVMABVP 2009


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HistoryPleaselistquestionsthatyouwouldliketoaskduringyourmedical

history.

1.2.3.4.5.6.7.8.9.10.

WhatClinicalDiagnosticsshouldbecompletedatthistime?

1.2.3.4.5.6.7.8.9.10.


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InitialDatabaseAvailable:

Tubes: PurpleTop RedTop

PackedCellVolume PCV: 24%(l) (2545%) TotalProtein 6.2 (5.07.5mg/dl)

CompleteBloodCount:

Test Findings Normal

WBC 7500 5,50019,500

Lymphocytes 1250(l) 15007000

Monocytes 1000 0850

Neutrophils 4500 250012500

Eosinophils 750 01500

Basophils 0 0100

RBC 6000 55008500

HCT 32% (l) 35 55%


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Chemistry:


Albumin 2.3 (l) 2.54.4g/dl

AlkPhos 143 20150IU/L

ALT 112 10118IU/L

Amylase 752 2001200IU/L

TBilirubin 0.5 0.10.6mg/dl

BUN

4

(l)

7

25

mg/dl

Calcium 9.2 8.611.8mg/dl

Phosphorus 5.6 2.96.6mg/dl

Creatinine 1.4 0.31.4mg/dl

Glucose 115 (h) 60110mg/dl

Na 149 138160mEq/l

K 2.8 (l) 3.75.8mEq/l

TP 6.2 5.48.2g/dl


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BasedonPhysicalExamandClinicalDiagnosticsthusfar,pleaseidentifya

problemlistforthepatient:

1.2.3.4.5.

6.7.8.9.10.11.12.13.14.

Pleaselistotherdiagnosticsthatneedtobecompleted:

1.2.3.4.5.6.


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Giventheconcernsofthepatient,whataresecondaryconcernsthatmedical

teammustmonitorfor?

1.2.3.4.5.

6.7.8.9.10.

STOP Therestofthecasewillprogressduringtheonlineclass.


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OnLineClassPortion: Pleaserevieweachdiagnostictestordered,copydown

theabnormalandlistconcernsbasedonthesefindings:

Clinical

Diagnostic

#1:

ProblemList:


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ClinicalDiagnostic#2:

ProblemList:


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ProblemList:


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ProblemList:


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ProblemList:


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Pleaselistacompletedproblemlistbasedonthecaseincludinghistory,physical

exam,andclinicaldiagnostics:

1.2.3.4.5.

6.7.8.9.10.11.12.13.14.15.

As we treat this patient, what are some monitoring diagnostics that will be

necessarytoevaluatetheeffectivenessofourtreatmentoptionsandconcerns

ofsecondarydiseaseconditions?

1.2.3.4.5


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SectionII: LectureNotes


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1/12/2010

Evaluating for Liver Damage and Dysfunction

Andrew J Rosenfeld, DVM ABVP

2009

Material Courtesy of Clinical Pathology for the Veterinary Team,

Rosenfeld, A and Dial, S. Wiley Blackwell, Ames Io, 2010

Case I : Pewter

Signalment: 20 kg MaleNeutered 5 year oldEnglish Bull Dog


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1/12/2010

Initial Triage Exam

Temp: 101.2 degrees Fahrenheit

Pulse: 160

Resp: 50-60 breaths / min

CRT: 2 secs

MM: Light Pink

Hydration: 8% dehydrated

Mentation: Depressed

Abdomen: Sore and painful to touch

History What should we ask?

1.2.3.4..

6.7.8.9.10.

Now What?

What should be in our clinical database?

1.

2.


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1/12/2010

Initial Database

Tubes:

Purple Top

Red Top

Packed Cell Volume

PCV : 34 % (L) (35-55%)

Total Protein: 6.0 (5.0-7.5 mg/dl)

Complete Blood Count


WBC 7500 5,500-19,500

Lymphocytes 1250 ( l) 1500-7000

Monocytes 1000 0-850

Neutro hils 4500 2500-12500

Eosinophils 750 0-1500

Basophils 0 0-100

RBC 6000 5500-8500

HCT 32% (l) 35-55%

Hemoglobin 11 (l) 9.5-15

Platelet 328000 200000-500000

Chemistry


Albumin 2.3 (l) 2.5-4.4 g /dl

Alk Phos 143 20-150 IU/L

ALT 112 10-118 IU/L

Amylase 752 200-1200 IU/L

T Bilirubin 0 5 0 1-0 6 mg/dl

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Problem List

1.2.3.4..

6.7.8.

9.10.

What other diagnostics are needed to be completed?

1.2.3.4.5.6.7.

8.9.10.

What are secondary concerns thatmedical team must monitor for?

1.2.

3.4.5.

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Introduction

As opposed to clinical diagnostic evaluation of renal diseaseand kidney function, the ability to evaluate liver damage vs.hepatic function is much more complex.

The goal of this chapter is to understand that patients with livertrauma have changes in liver enzymes. However, this does notalwa s mean the liver is non-functional.

The other concern is that a patient with have severe debilitating liver disease with poor function, can have bloodwork parameters within normal limits.

Team members must be able to understand the importance andthe limitation of hepatic clinical diagnostics when approaching apatient with potential liver disease.

Liver Physiology

The liver has many functions inthe body; the most important isdetoxification of toxins.

The small intestine absorbs allfood stuffs, microbes and toxinsinto a large venous system called

e or a enous ys em.

The large portal vein carries all ofthese substances into the liverwhere intracellular chemicals(enzymes) detoxify toxins intoinert waste products.

Liver Detoxification

For the liver to be able to detoxifyblood, the internal architecture ofthe liver must be adapted to filterblood, harvesting necessarynutrients and removing toxins.

To do this the liver architecture is

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Liver Detoxification The nutrients are absorbed,

altered into other proteins,energy and fats needed by thebody and then released backinto the blood venous flow forgeneral circulation.

The toxins and bacteria aredeactivated and then releasedinto channels, called Canniculi,running between layers ofhepatocytes.

These canniculi lead to the bileductules, which then move alldeactivated sludge and debrisinto the gall bladder.

Liver Detoxification If the body is unable to detoxify these compounds, the active toxins can build

up into the blood stream and tissues.

This can produce anorexia, weakness, weight loss, vomiting and diarrhea.

Further specific toxins can penetrate the central nervous system producingneurologic symptoms such as

Seizures

Acute blindness

Circling

Head pressing

Abnormal behavior

Neurologic symptoms produced secondary to decrease hepatic function iscalled Hepatic encephalopathy.

Since this process is stimulated by the absorption of nutrients and improperdetoxification of toxins, neurologic signs can be closely associated withfeeding.

Liver Production

The liver produces many of the bodys building blocksnecessary for normal maintenance, growth andproduction. Of these factors, the liver produces

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Risks of patients with reduced hepatic function

Issues with Detoxification:

Hepatic Encephalopathy:Development of neurologicsymptoms secondary toimproper detoxification of

remain in the body affectingthe central nervous system.

Physical Symptoms due tobuild of toxins and bilirubin:Increased toxins can produce

nausea, anorexia, depression,vomiting, diarrhea, weaknessand weight loss.


Alteration in Protein Production

The liver also produces a protein molecule called albumin.

Albumins function is to carry other molecules and hormones around the bloodstream in a deactivated form until the body requires the chemical.

In order to move albumin through the blood stream, large amounts of fluid mustibe pulled from the tissue.

This physiological draw of fluid that albumin exerts on the tissue is calledOncotic Pressure.

Loss of albumin production secondary to liver dysfunction can decrease oncoticpressure, increasing the amount of fluid returning to the tissue.

If severe, large amounts of fluid accumulation can occur within the abdomen(ascites). Further medical team members must be extremely cautious withhospitalize patients on intravenous fluids with low albumin levels since thesepatients have increased risk of pushing larger amounts of fluids into the tissue.

This increases risks of moving fluid into lung tissue producing pulmonary edemaand developing fluid overload.


Decreased Production:

Anemia:

Due to lack of Red Blood Cell precursors.

A i l ith h i h ti di d l

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Liver Function Concern of Dysfunction

Detoxification

Hepatic Encephalopathy: Development of neurologic symptoms secondary to improper

detoxification of microbes and toxins which remain in the body affecting the central

nervous system.

Physical Symptoms due to build of toxins and bilirubin: Increased toxins can

produce nausea, anorexia, depression, vomiting, diarrhea, weakness and weight loss.

Formation of Building Blocks

Anemia: Lack of Red Blood Cell precursors

Increased Clotting Time: The liver produces clotting factors that finalize clot formation.

Hypoalbunemia: Due to lack of blood albumin, the body can shift fluid from the vascular

supply to the tissue, increasing fluid accumulation in the body producing ascites, edema

and pulmonary edema (with patients on IV fluids).

Glucose Storage Hypoglycemia (rare)

Causes of Liver Disease

Infectious Liver Disease: Viral, bacterial, fungal and parasites

pathogens can infect and invade normal liver tissue producing

acute or chronic disease and debilitation

Inflammatory Disease: Hepatitis is the activation of the immune

system by some foreign antigen within the liver. This antigenic

stimulation produces an influx of white blood cells through healthy

liver causing damage and irritation. Inflammatory disease can be

acute, chronic or end stage ( Cirrhosis).

Cancer (Neoplasia): The liver is both the site of primary cancer

and a common site of secondary metastatic disease. Some

common cancers that primarily affect the liver are Hepatic

Adenocarcinoma, Hepatic Cholangioadenocarcinoma, Lymphoma,

and Mast Cell tumor.

Causes of Liver Disease

Metabolic Disease: This form of liver disease occurs as inert

compound build-ups within the liver, destroying the normal

architecture and liver function. Common metabolic diseases of the

liver include:

Hepatic Lipidosis: This disease syndrome occurs

commonly in the cat and horse (pony) when these animals

have a diseases entity that produces a profound anorexia.

The animals shunt large amounts of fat into the liver to

transform it into sugar. The movement of fat into the liver is

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Identifying Liver Damage vs. Hepatic Dysfunction

Within the liver cells are enzymes that function to change or produce specific body buildingblocks or detoxify toxic chemicals in the body. Clinically we evaluate the following intracellularenzymes:

Alanine aminotransferase (ALT)

Aspartate aminotransferase (AST)

Gamma-Glutamyltransferase (GGT)

Alkaline Phosphatase (Alk Phos)

Unlike evaluating kidney disease by monitoring azotemia, these clinical diagnostics do notrepresent a build up toxin, but rather normal enzymes produced within the hepatocytes.

Normally, a specific level of each enzyme leaks from the hepatocyte into the blood stream.

Acute trauma to hepatocytes can produce sharp elevations of liver enzymes. Increases inthese liver enzymes support liver trauma, but do not always suggest liver dysfunction.

However, with chronic to end stage disease, there may enough hepatic enzymes withinthe blood stream to produce normal blood levels in clini cal testing, but the liver maynot be functional.

Liver Damage Enzymes

ALT (Alanine aminotransferase):

Alanine aminotransferase (ALT) is responsible for the conversion of 2-oxoglutarate to pyruvate and glutamate in the liver cells (hepatocytes).

The following patterns in the ALT level can be observed:

Low ALT activity is not generally associated with disease conditions.

Increased activity of the enzyme in the blood occur when there arealterations in the lipid membrane of the hepatocytes, secondary toinjury, inflammations or infection within the liver.

The increase blood levels do not indicate the severity of thedamage to the hepatocytes or degree of reversibility of thedisease process.

Further ALT activity can also be increased secondary to:

Chronic use of anticonvulsants, steroids and other drugs

Physical trauma Cardiac Disease


Aspartate aminotransferase (AST or SGOT): Aspartate aminotransferase (AST) isan intracellular enzyme in all cells, but has higher levels of activity in muscle and livercell damage. The following patterns in the AST level can be observed:

Decreased AST activity: Low ALT activity is not generally associated withdisease conditions.

Increased AST activity: As with ALT, AST blood levels in the blood occur when

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Liver Damage Enzymes Gamma-glutamyltransferase (GGT): Gamma-glutamyltransferase is

more an indicator of gall bladder obstruction or lack of bile flow. GGT isan intracellular enzyme responsible for cleaving C-terminal glutamylgroups from one substrate or molecule to another, and is thought to beinvolved in pathways used to protect cells from oxidative injury. GGT ispresent in all cells except it has higher concentration in renal epithelial,bile duct and hepatic cells.

The followin atterns of GGT levels can be observed:

Decreased GGT activity: Low GGT activity is not generallyassociated with disease conditions.

Elevations in GGT:

Increased GGT activity can be associated with decreased bile

flow (cholestasis)

Unlike AST and ALT, GGT does not leak from hepatocytes; itsactivity is increased due to increased production (induction) ofthe enzyme in response to disease.


Alkaline Phosphatase (SALP or ALP): Alkaline Phosphatase is present within theliver, intestine, bone, kidneys and placenta. On most chemistry panels, Alkaline

Phosphatase activity represents the combined activity all combined tissue alkalinephosphatase levels. The following patterns of ALP can be observed:

Decreased ALP activity: Low ALP activity is not generally associated withdisease conditions.

Increased Alkaline Phosphatase activity: High ALP can originate fromdiseases and non-diseased conditions. Similar to GGT, ALPs activityincreases because of increased production of the enzyme (induction) in

response to disease. Some conditions that increase Alkaline Phosphataseactivity are:

Hyperadrenocorticism Liver and Gall Bladder Disease

Long Term Medication

Bone growth

Liver Dysfunction Enzymes

Bilirubin:

Bil irubin is a toxic metabolite

produced from the red blood cell

destruction in the spleen and thebreakdown of hemoglobin.

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Liver Dysfunction Enzymes Bilirubin:

The buildup of bilirubin in the serum

and body in association with liverdisease indicates liver dysfunction.

However, it should be noted that

although patients that are ictericsecondary to liver disease have

liver dysfunction; however not all

patients with liver dysfunction areicteric.

Further, increase levels of Bilirubin

also can be associated with increaseintravascular red blood cell destruction

(e.g. Immune-mediated Hemolytic

Anemias) or gall bladder obstruction.


Blood urea nitrogen (BUN):

A low BUN level can be associated with the livers inability to produce take ammonia moleculesand produce BUN. Whenobserved on clinical diagnostics, it may suggest a liver dysfunction.

A low BUNby itself doesnot alwaysindicateliverdysfunction. Low protein diets can alsoresult in a low BUN.

Albumin:

Albumin is a small carrier protein that binds to hormones and other components in the bloodstream to maintain and move necessary elements throughout the body.

Decreases in blood albumin concentration can occur generally with a number of diseasesyndromes that effect production or loss of the protein molecule.

A decrease in functioning hepatocytes will compromise the livers ability to produce albumin. As ageneral rule, at least 75% of normal liver function must be lost before albumin concentration is

decreased.

When attributable to liver disease, hypoalbuminemia can be an indicator of altered liverfunction.

However, low body albumin can also be associated with Kidney disease, bleeding and intestinaldisease.


Bile Acids

Hepatocytes also produce chemicals called bile acids that help to emulsifyfat within the small intestine.

Bile acids are stimulated when the patient eats.

Bil id th t th h th ll bl dd d i t th bil

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Hepatic Clinical Diagnostics Since liver disease, trauma and dysfunction can be difficult to

evaluate based on blood work alone, the medical team must alsoevaluate the history, physical examination and other diagnostic aids.

There are many potential forms of liver disease, blood work can

appear normal and there can still be significant liver dysfunction.

Further, clinical diagnostics and imaging alone are often notsufficient to diagnose the cause of the liver disease present.

If the medical team determines that hepatic dysfunction is occurring,a liver biopsy (fine needle, tissue biopsy, or core biopsy) may be

recommended to obtain a final diagnosis and help outline treatmentprotocols.

Hepatic Clinical Diagnostics Complete Blood Count: Components of the complete blood count can vary dependent on the form of

liver disease; however general trends should be monitored for:

Red Blood Cells:

With chronic waning disease, chronic anemia may be present secondary to the lack ofprecursors for cellular components.

Also chronic liver disease can affect the patients ability to clot blood.

With significant anemia, platelet number, clotting times and a blood film should be evaluatedto determine if the patient has a non-regenerative anemia vs. chronic bleeding concerns.i i i i i i l i

White Blood Cells:

With concerns of infectious disease, changes in white blood cells should be evaluated.

With certain forms of cancer (i.e. hepatic lymphoma), white blood cell elevations can besevere with extremely abnormal cytology and high white blood cell.

Platelets:

With concerns of decreased clotting factors and an inability to finalize the clotting process(coagulopathy), platelets counts should also be closely monitored.

Animal should be carefully assessed for bruising, and jugular sticks should not beattemptedif t here is concern of a coagulopathy.

Hepatic Clinical Diagnostics

Blood Film:

Changes in Red Blood CellMorphology

Acanthocytes / Echinocytes

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Hepatic Clinical Diagnostics Chemistry:

Liver Damage Enzymes:

ALT

AST

GGT

Alk Phos

Liver Dysfunction Enzymes:

Elevated Total Bilirubin

Paired Bile Acids

Hypoalbunemia (Suggestive)

Low Blood Urea Nitrogen (Suggestive)

Hypoglycemia (Rare)

Urinalysis

A urinalysis should always accompany all blood work evaluations to help determine and indicatemultiple organ issues. Key concepts to monitor are:

Urine Specific Gravity: Determine Renal Azotemia vs. Pre-renal Azotemia

Bilirubinuria:

Dog urine can have trace to 1+ bilirubin with no underlying disease. Althoughbilirubinuria can be found in normal dog urine, it should not be completely discounted.Bilirubinuriawill be seen before hyperbilirubinemia in dogs with early hepatic disease.

In cats, the presence of bilirubin in feline urine is always significant. The diseases thatcause of bilirubinuria are the same as those that result in hyperbilirubinemia; liverdisease, hemolysis, bile duct obstruction and sepsis.

Urine Sediment:

Ammonium Biurate Crystals can be seen in neutral to high urinary pH and areassociated with liver disease and portocaval shunts. However this can be a normalfinding in Dalmatians.

Bilirubin crystals are seen in any urinary pH and are associated with liver disease andimmune-mediatedhemolytic anemia


Coagulation Screen: Evaluating clotting times (Activated Clotting Time (ACT),Partial Thromboplastin Time (PT), Activated Partial Thromboplastin Time(APTT)) can help detect early trends of the patients ability to clot blood.

Blood Gas: As discussed in Renal Course of Abaxis University, a metabolicacidosis can be produced by disease which decrease glomerular filtration, increasetoxins and toxic metabolites and increase the loss of bicarbonate rich fluids. Sinceliver disease can produce all these components, a metabolic acidosis can be

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Abdominal Radiography: Abdominal radiographs can help assess for changes inhepatic size and shape, evidence of gall bladder for stones (Cholelithe), and any other

changes in the abdomen that can suggest serious disease.

Abdominal Ultrasound:

Abdominal ultrasound can assess the internal architecture of the abdominal organsfor changes suggestive of focal or diffuse hepatic disease, changes in the gallbladder wall suggestive of infection or obstruction, and identification of abnormalblood vessels that could suggest a Porto-caval shunt.

It is important to note that changes in hepatic architecture can only suggestfocal or diffuse disease and rarely helps the medical team confirm diagnosis.

Cellular or tissue biopsy is possible through ultrasound guided biopsy techniques.

Exploratory Surgery: In some cases, when ultrasonic biopsy or fine needle aspirate isnon-diagnostic, exploratory or laparoscopic surgery and wedge or core biopsy of the livermay need to be completed.


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SectionIII: Appendix

Ab i U i i A di


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AbaxisUniversityAppendix

EvaluatingforLiverDamageandDysfunction

A.Rosenfeld,DVMABVP 2009

TableI: SecondaryConcernsofLiverDysfunction

LiverFunction ConcernofDysfunction

Detoxification

Hepatic Encephalopathy: Development of neurologic symptoms secondary to

improperdetoxificationofmicrobesandtoxinswhichremain inthebodyaffecting

thecentralnervoussystem.

Physical Symptoms due to build of toxins and bilirubin: Increased toxins can

produce nausea, anorexia, depression, vomiting, diarrhea, weakness and weight

loss.

FormationofBuildingBlocks

Anemia: LackofRedBloodCellprecursors

Increased Clotting Time: The liver produces clotting factors that finalize clot

formation.

Hypoalbunemia: Due to lack ofbloodalbumin, the body can shift fluid from the

vascular

supply

to

the

tissue,

increasing

fluid

accumulation

in

the

body

producing

i d d l d ( i h i IV fl id )


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ascites,edemaandpulmonaryedema(withpatientsonIVfluids).

GlucoseStorage Hypoglycemia(rare)

TableII: EnzymeswhichevaluateLiverDamage

Alanine

aminotransferase

(ALTorSGPT)

Alanine aminotransferase (ALT) is responsible for the conversion of 2oxoglutarate to pyruvate and

glutamateinthelivercells(hepatocytes).

NormalLevel:

Canine: 670IU/L

Feline: 2876IU/L

ThefollowingpatternsintheALTlevelcanbeobserved:

LowALTactivityNotassociatedwithdiseaseconditions

Increasedactivityoftheenzymeoccurswith:

ACUTELIVERDAMAGE

ChronicDrugTherapy(Anticonvulsants,Steroids)

PhysicalTrauma

CardiacDisease

Aspartate

aminotransferase

(ASTorSGOT)

Aspartateaminotransferase(AST)isanintracellularenzymeinallcells,buthashigherlevelsofactivity

inmuscleandlivercelldamage.

NormalLevel:

Canine: 1043IU/L

Feline: 12 40 IU/L


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Feline: 1240IU/L


LowASTactivityNotassociatedwithdiseaseconditions


ACUTELIVERDAMAGE

Disease,whichaffectthemuscularskeletalsystem(e.g.traumaorseizure)

Disease,whichproduceredbloodcelldestruction(e.g.ImmuneMediatedHemolytic

Anemia),sincethereissignificantlevelsofASTinredbloodcells.

Gamma

glutamyltransferase

(GGT):

Gammaglutamyltransferase (GGT): Gammaglutamyltransferase is more an indicator of gall bladder

obstruction or lack of bile flow. GGT is an intracellular enzyme responsible for cleaving Cterminal

glutamyl groups fromonesubstrateormolecule toanother,and is thought tobe involved inpathways

usedtoprotectcellsfromoxidativeinjury.GGTispresentinallcellsexceptithashigherconcentrationin

renalepithelial,bileductandhepaticcells.

NormalLevel:

Canine: 08IU/L

Feline: 01 IU/L


LowGGTactivityNotassociatedwithdiseaseconditions


ACUTELIVERDAMAGE

IncreasedGGTactivitycanbeassociatedwithdecreasedbileflow(cholestasis)

UnlikeASTandALT,GGTdoesnotleakfromhepatocytes;itsactivityisincreaseddueto

increasedproduction(induction)oftheenzymeinresponsetodisease.

Alk li Ph h (SALP ALP) Alk li Ph h i i hi h li i i b


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AlkalinePhosphatase

(SALPorALP):

AlkalinePhosphatase(SALPorALP):AlkalinePhosphataseispresentwithintheliver,intestine,bone,

kidneysandplacenta. Onmostchemistrypanels,AlkalinePhosphataseactivityrepresentsthe

combinedactivityallcombinedtissuealkalinephosphataselevels.

NormalLevel:

Canine: 876IU/L

Feline: 862 IU/L


LowAlkPhosactivityNotassociatedwithdiseaseconditions

IIncreasedAlkalinePhosphataseactivity: HighALPcanoriginatefromdiseasesandnondiseased

conditions.SimilartoGGT,ALPsactivityincreasesbecauseofincreasedproductionofthe

enzyme(induction)inresponsetodisease.SomeconditionsthatincreaseAlkalinePhosphatase

activityare:

Hyperadrenocorticism

LiverandGallBladderDisease

LongTermMedication

Bonegrowth


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syndromesthat effectproductionorlossoftheproteinmolecule.


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y p p

A decrease in functioning hepatocytes will compromise the livers ability to produce

albumin. Asageneralrule,atleast75%ofnormalliverfunctionmustbelostbeforealbumin

concentrationisdecreased.

Whenattributabletoliverdisease,hypoalbuminemiacanbeasuggestionofalteredliver

function.

However, low body albumin can also be associated with Kidney disease, bleeding and

intestinaldisease.

Bloodureanitrogen

(BUN)

AlowBUNlevelcanbeassociatedwiththeliversinabilitytoproducetakeammoniamoleculesandproduceBUN. Whenobservedonclinicaldiagnostics,itmaysuggestaliverdysfunction.

AlowBUNbyitselfdoesnotalwaysindicateliverdysfunction. LowproteindietscanalsoresultinalowBUN.

BileAcids

Hepatocytesalsoproducechemicalscalledbileacidsthathelptoemulsifyfatwithinthesmallintestine.

Bileacidsarestimulatedwhenthepatienteats. Bileacidsthenemptythroughthegallbladderandintothecommonbileduct. Afterfatisemulsified,bileacidsarethenrapidlyreabsorbedbythesmallintestine.

NormalLevel:

Canine: Preparandial:05.0mol/l PostParandial: 3.912.7mol/l

Feline: Preparandial:05.0mol/l PostParandial: 5.010.0mol/l

AlterationsinBileAcidscanindicateatrueliverdysfunction.

TableIV:SuggestedOverviewofClinicalDiagnosticsofLiverDz


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gg g

Completebloodcount

Redbloodcellcount: ElevationsofHCT/PCVDehydration,ConcernsofChronicAnemia

White

Blood

Cell

Count:

Bacterial,

fungal,

parasitic

or

protozoal

causes

of

infectious

hepatic

disease,

leukocytosis

Platelets: LowPlateletcountcansupportchronicbleedingsecondarytodecreasedclottingfactors,

thrombocytopenia.

BloodSmear: NonregenerativeAnemiaduetosecondarytolackoferythropoietin,possibledecreased

plateletnumber,andredbloodcellabnormalities(Acanthocytes/Echinocytes,BurrCellsHepatic

Lipidosis,Schistocytes)

Bloodchemistry

LiverDamage

(SeeTableII)

AST

ALT

ALKPHOS

GGT

Bloodchemistry

LiverDysfunction

(SeeTableII)

TotalBilirubin(HepaticDisease)

LowAlbumin(HepaticDisease)

LowBUN

+/

Blood

Glucose

ElevationsinPostParandialBileAcids

Urinalysis

UrineSpecificGravity(USG): tohelpdifferentiaterenalfromprerenalazotemia

UrineStick:Bilirubinuria: >+1(Canine) />Trace(Feline)

UrineSediment: AmmoniumBiurateCrystals&Bilirubincrystals

Elevationsin:


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CoagulationProfile

ActivatedClottingTime(ACT)

PartialThromboplastinTime(PT)

ActivatedPartialThromboplastinTime(APTT))

BloodGas

MetabolicAcidosis Thefollowingparametersareobservedwithmetabolicacidosis:

BloodpH


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OtherPossible

DiagnosticExams

shape,evidenceofgallbladderforstones(Cholelithe),andanyotherchangesintheabdomen

thatcansuggestseriousdisease.

AbdominalUltrasound:

Abdominalultrasoundcanassesstheinternalarchitectureoftheabdominalorgansfor

changessuggestiveoffocalordiffusehepaticdisease,changesinthegallbladderwall

suggestiveofinfectionorobstruction,andidentificationofabnormalbloodvesselsthat

couldsuggestaPortocavalshunt.

It

is

important

to

note

that

changes

in

hepatic

architecture

can

only

suggest

focal

or

diffusediseaseandrarelyhelpsthemedicalteamconfirmdiagnosis.

Cellularortissuebiopsyispossiblethroughultrasoundguidedbiopsytechniques.

ExploratorySurgery: Insomecases,whenultrasonicbiopsyorfineneedleaspirateisnon

diagnostic,exploratoryorlaparoscopicsurgeryandwedgeorcorebiopsyofthelivermayneed

tobecompleted.


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Evaluating Liver Disease and Dysfunction

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