The document provides information about the liver anatomy and functions in various animal species. It discusses the liver's role in metabolizing hemoglobin and bilirubin, maintaining glucose homeostasis, processing amino acids and lipids, detoxifying ammonia, storing vitamins and producing clotting factors. Common liver diseases mentioned include infectious hepatitis, cirrhosis, and red water disease caused by Clostridium haemolyticum bacteria. A number of liver function tests and their reference ranges in different animals are also outlined.

1. Dr SUMREEN KOUR
MVSc Scholar

2.  Largest internal organ
 Position: placed in rt side of
abdominal cavity in oblique
downward & forward
direction.
 Extends from lumbocosto
angle to level of 7th-8th rib.
 Size:
 Herbivores-1.5%bwt
 Omnivores-2-3%bwt
 Carnivores-3-5%bwt
 Remarkable capacity to
regenerate portal blood.

3.  Origin:
• derived from outpocketing of endoderm.
 Lobes:
 left lateral lobe,rt lateral lobe,left medial,rt
medial,quardate, caudate & papillary.
 Ligaments:
• Falciform ligament.
• Rt lateral ligament.
• Round ligament.
• Caudate ligament.
• Lesser omentum.

4.  Consists of three vessels:
1. A branch of hepatic artery.
2. A branch of portal vein. sinusoids
3. A tributary of bile duct.
central vein
hepatic vein

7.  Breakdown of haem produces bilirubin & other
bile pigments.
 Bilirubin must be made water soluble to be
excreted out.
 Occurs in 4 steps:
1. FORMATION.
2. PLASMA TRANSPORT
3. LIVER UPTAKE
4. CONJUGAION
5. EXCRETION

8. Hemoglobin
Heme
Biliverdin
Bilirubin
MPS
CELL
Globulin
Iron
Reutilized
Bilirubin diglucuronide
Bile
LIVER
Urobilinogen
Stercobilinogen
Urobilin
Stercobilin
Excreted
in faeces
INTESTINE
Enterohepatic
circulation
Urinary urobilinogen
KIDNEY
Hb is a conjugated protein consisting of
4 heme molecules (Ferroprotoporphyrin)
linked to protein called globulin.
(esterification)
(colorless)
(colon)
(oxidized)

9.  Major function of liver is to maintain glucose
homostasis.
• Liver responds to hormonal cues to breakdown
or synthesize glycogen /sythesize glucose.
 Control:glucagon
epinephrene
corticosteroids.
Functions:
• Storage of large amount of glycogen.
• Conversion of galactose & fructose to glycogen.
• Gluconeogensis.

10.  Deamination of amino acids.
 Formation of urea for removal of ammonia
from body.
 Formation of plasma proteins.(albumin).

11.  Liver has several functions in lipid
metabolism.
 Plasma fatty acids released from adipose
tissue are extracted by hepatocytes
 triglycerides(beta oxidation).
 Liver also extracts chylomicron remenanats
& LDLP from plasma—( major route of
cholestrol entering liver)

12.  Liver is responsible for majority of ammonia
detoxification.

 bacterial degradation of amines.
 amino acids
 purines(urease)
 portal circulation
 renal excretion
GIT
AMMONIA
Detoxified
•either by conversion in
urea(kreb cycle).
•Comsumption in synthesis of
glutamine

13.  Liver acts as store
house of various
vitamins.
 Liver also synthesize
clotting factors.
 Liver is site of vit-K
dependent activation
factors II, VII, IX, X
 Liver also stores iron as
ferritin.
 Hepatic cells contain
large amount of
apoferritin.
 When iron is in excess
amount+ apoferritin
ferritin (stored
in hepatic cells) & thus
acts as BLOOD IRON
BUFFER.

14.  Defencesive & detoxification:
 Kuffer cells(pahocytosis) of liver play impt role.
 Liver removes or excretes drugs,hormones & other substance.
 Drugs:sulphonamide
 pencillin
 ampicillin
 erythromycin
 Calcium from body is excreted by liver---bile—gut-faeces.

15.  Bile acids are composed of cholestrol,bile
salts & steriods.
 Main bile acids are:cholic acid
 Conjugated to taurine & glycine in liver so
they exist in ionised form as bile acids.

16. SIGN PATHOGENSIS OTHER CAUSES
ICTERUS •Less commonly seen
in cattle unless
billiary blockage
occurs.
•Failure of
uptake,conjugation
or excretion of
bilirubin.
•Massive
hemolysis(neonatal
isoerythrolysis
,bacillary
hburia,anaplasmosis).
•Bile duct blockage.
WEIGHT LOSS •Common.
•Anorexia.
•Failure of metabolic
function of liver.
•Many causes

17. DIARRHEA •Especially cattle with
chronic liver disease.
•Related to portal
hypotension &
increased hydrostatic
pressure.
•GIT disease.
•Systemic disease.
•Septicemia.
ASCITES •Calves with liver
cirrhosis.
•hypoalbuminemia,porta
l hypertension caused by
venous blackade
&increased hydrostatic
pressure & protein
leakage to peritoneum.
•Cardiac failure.
•Hypoproteinemia.
•Cushing syndrome.
CHANGE IN FECAL
COLOR
•Young animalsimple
digestive tracts-
stercobilin-metabolite
of bilirubin.
•Cholestasis-lighter fecal
colour.

18. DERMATITIS:
•Occurs because of hepatic Photosensitization(type 3).
•Caused by photodynamic substance-phylloerythrin.
•Normal end product of chlorophyll metabolism-phylloerythrin
•Formed by bacterial degredation of chlorophyll in GIT.
•
Normally phylloerthrin is secreted into intestine by billiary system &
excreted in faeces.
•
•Damage to this mechanism prevents excretion of phylloerythrin
allowing PS to enter circulation &accumulate in skin.
•This condition is exacebrated by hepatic parasites..

20.  These include:
• Hyperexcitability.
• Convulsions.
• Muscular tremors & weakness
• Dullness
• Compulsive walking.
• Head pressing.
• Circling.
• Coma.

21.  Causes:
 hypoglycemia
 accumulation of excess amino acids &
ammonia.

23.  Change in liver size.
 Tenesmus.
 Pain.
 Haemmorages(factors 2,5,7,9&10).
 Pruritis.

24.  Selection of a particular liver function test as a
reliable index is difficult because of many
limitations.

One specific function of liver may be effected by
a no of extrahepatic conditions.
 Extensive damage of liver is required to keep
the test positive.
 The tests lacks in sensitivity.
Therefore single test does not present the status of
whole liver.

25. dogs 5.8-6
cattle 8.4-9.8
Horse 15.2-18
sheep 6.8-10.7
buffalo 7.1-9.8

26. Conjugated bilirubin or soluble bilirubin or
Direct bilirubin when comes in contact with
Ehrlich`s diazo reagent, gets diazotized and
there upon produces “azobilirubin” the
color of which is red.
Unconjugated bilirubin is water insoluble and
therefore produces color only after addition
of methly alcohol to make it soluble.
Unconjugated bilirubin = Total bilirubin -
Conjugated bilirubin

27. species Conjugated(mg/dl) Total
bilirubin(mg/dl)
Dog 0.14 1.0-10.0
Cattle 0.18 1.9
Horse 0.10 0.2-6.0
Sheep 0.12 0-0.4
Interpretation:
Cattle:In generalized liver disease maximum bilirubin will not exceed
3.5 mg/dl due to large functional reserves of bovine liver for excretion
of bilirubin.

28. One of several Vit. K dependant
coagulation factors synthesized by liver
Species Normal clotting
time
Sheep 2 minutes
Dog 2-3 minutes
Cattle 7 minutes
Horse 11 minutes.
Interpretations: Prolonged time could be due to
-Decreased hepatic cell mass (extensive necrosis/
cirrhosis)
-Cholestasis (insufficient bile for absorption of fat soluble
vitamin)

29.  BROMOSULPHTHALEIN CLEARANCE TEST:
 In large animals this test is mostly used.
 In this test 500-1000mg of BSP is injection I/v.
blood sample is taken before the injection & 4 times 5-
12min following injection(5,7,9,11min).
samples are analysed for for color produced by BSP. & half
life determined by plotting graph.
HALF LIFE:
Normal horses-3.5min.
Ruminants-5min

30. Sorbitol
dehydrogenase(SDH).
L-iditol
dehydrogenase(ID).
•Indicator of liver damage.
•Preferred in cattle & sheep.
•Abundant in liver,kidney, muscle,myocardium.
Aspartate
aminotransferase(AST).
SGOT or
Alanine
aminotransferase(ALT).
SGPT
•Indicator becaues of high level in liver.(non-
specific).
Arginase •Specific indicator in hepatic diseases.*
•Short half life –acute hepatic disease.
Glutamate
dehydrogenase(GD)
High conc in serum of ruminants & horses.

31. Ornithine
carbamoyl
transferase (OCT)
•Elevated level in chronic disesases(active
liver necrosis).
Alkaline
phosphatase(ALP)
•horses
Gamma
glutamyltransferase
(GGT)
•Activity highest in kidney,pancreas & liver in
equines.
•Also used in cattle, sheep .

32. ENZYMES CATTLE(unit/l) HORSE(unit/l)
ALT/SGOT 11-40 3-23
AST/SGPT 78-132 220-600
ALP 0-500 140-4003
GGT 6.1-17.4 4-44
LDH 692-1445 160-410
SDH 4.3-15.3 1.9-5.8
ICH 9.4-21.9 5-18

33.  CATTLE:
 GGT
 ALP
 AST useful in chronic hepatitis disease.
 GD
 SDH effective & sensitive in early stages of hepatic
dysfunction.
Glutamate dehydrogenase :This is enzyme
of choice for cattle as it is much more
sensitive than transaminase.

34. Remove primary reason
Provide CHO rich diet
Restrict protein
Provide rest to animal
Water soluble vitamins
Provide vitamin K
Choline

35. Cholegogues:cholekinetcs&
cholerectics
Sedatives like Xylazine
metronidazole
steroids
Diuretics & laxatives

37.  Inflammation of hepatic cells.
 May be acute or chronic.

38.  INORGANIC POISONS:
• Copper , phosphorous,
arsenic, possibly
selenium.
 ORGANIC POISONS:
• Carbon tetrachloride,
• hexachloride,gossypol,cr
esols & coal tar
pitch,chloroform.
 POISONOUS PLANTS:
• Weeds: Senecio,
Crotolaria , Heliotropium.
• Pasture & cultivated
plants:lupins,Alsike
clover,water damaged
alfa-alfa hay.
• Trees & shrubs: lantana
camara,myoporum spp.
 FUNGUS:
• fusarium sp, Penicillium
rubrum, Aspergillus flavus.
 INSECTS : sawfly larvae

39. INFECTIOUS HEPATITIS PARASITIC CAUSES
 Virus of rift valley
fever.
 Chlymadia sp.
 histoplasmosis
 Liver flukes.
 Migrating ascaris.

40.  Sustained Inflammatory process within liver.
 ETIOLOGY:in domestic animal is not known bt
however toxins play major role.

41.  RED WATER DISEASE
 ICTEROHAEMOGLOBINURIA
o Bacterial disease- Anerobic Cl. Haemolyticum
(cl novyi type D).
o Soil borne anerobe growing bacteria in liver.
o Affects cattle.
o Highest incidence is seen in ruminants consuming forages in
area with snail.
o

42.  Spores of Cl. Haemolyticum are transported by blood &
lymph to body tissue & organs.
 Pre-requisite: Host
Presence of toxins
Inflammation/necrosis*.
Result in formation of hypoxic milieu favourable for
spore germination & growth of toxin producing
vegtative cells.
Migrating fluke are primary
factors leading to liver necrosis &
anerobic condition.

43.  Vegetative cells releases toxins(necrotoxin &
hemolytic )
 Causes necrosis of surrounding tissue & allowing
infection.
 There is development of organised thrombus in
subterminal branch of portal vein producing infarct
which is characteristic of this disease.
 Most of bacteria grow in this anerobic env
producing toxin.

44.  Causing:toxemia
vascular damage
intravascular haemolysis.
Principle toxin produced is is beta
toxin(phospholipase C) highly lethal.

45.  EARLY SIGNS:
• CNS depression.
• Anorexia.
• Segregation of affected afected
animal.
• Rumination & lactation ceazes.
• Initially tempt is 104-106’F but
declines to normal or below
before death.
• Breathing is
rapid,shallow,distresed.
• Blood tinged froth from
nostrils,mouth.
 LATE SIGNS:
 If animal survives after 24hrs,
• Wine coloured
urine(hemoglobiunuria)
• Anaemia.
• Icterus.
• Juglar vein pulsation.
• Blood is thin & coagulates
slowly..
• s/c odema of ventral areas
seen.

46. •Infarcts in liver
•Blackish kidney

47.  Common lesions:necrosis & hemogloburia.
 Rigor mortis devlops early.
 Anaemic infarct* in liver.(pathagnomic)
Gall bladder: dark coloured
granular appearance of bile.
adult fluke in bile duct.
spleen: enlarged & haemorrages.
Urinary bladder: dark red urine.
In pregnant female: uterus has haemorrages.
amniotic fluid is red.
Trachea & bronchi:blood tinged & frothy exudate.
Cardiac muscle: congested
Peritoneal,pleural & pericardial cavities:serosanguineous fluid.

48. leptospira All ages cattle on
pasture
•Acute fever
•Red coloured
milk
•Hburia
•May die 24-48hrs
Leptospira titre
Postpaturient
hburia
Lactating cows 4-
6wk pp
•Acute
•No changes in
milk
•No fever
•Die in 12-48hrs
•hburia
hypophosphatemia
babesiosis Enzootic area
Tick borne
Young animals
•Fever
•Jaundice
•Abortioncourse 2-
3wk
•hburia
Blood smear
Complement
fixation test
Chronic cu
poisoning
Long term oral
adm of medicine
Jaundice
No fever
hburia
Acute haemolytic
anaemia

49.  TREATMENT:
 Penicillin-20000I/M
or
Tetracycline-10mg/kgbwt
I/M
 Blood transfusion
 Vitamin & iron
supplementation.
 PREVENTION:
 Vaccination
 Commercial
bacterin/toxoids.
 Immunization 2dose 3-
4wk apart.

50.  Caused by :
 Fasciola hepatica in
ruminants.
 Cattle develop degree of
resistance to repeated
infections,but sheeps do
not.
 Fasciola magna:infection
do not become patent in
cattle as fluke are
surrounded by capsules.
 Dicrocoelium dendriticum

51. Young migrate to hepatic parenchyma
Bile duct doubles size
Adult cattle & sheep act as carrier.
IH:snails lymnaeid –infective
metacercaria

52.  ACUTE
 After entry of hepatic fasciolasis in liver parenchyma
clinical signs appear 5-6wks after ingestion of
metacercaria.
 Quiescent spores of Cl.novyi become activated in anerobic
condition created by Fasciola hepatica causing infectious
necrotic hepatitis.

53.  CHRONIC:
 Adult fluke in bile duct
 Causes: cholangitis
 biliary obstruction(due to high proline)
 fibrosis
 leakage of plasma protien across epithelium –
 hypoalbunemia

 anaemia*

 Increases susceptibility of Salmonella dublin

54.  NECROPSY:
 Acute:
 swollen liver
 Perforation & subscapular
& haemorrage
 Parenchyma is damaged
& friable.
 Chronic:
 Leaf like flukes &
thickened bile duct
 Calcification of bile duct
in cattle

56.  DIAGNOSIS:
 Fecal examination.
 ELISA & DOT ELISA
 TREATMENT:
• Albendazole @5mg/kgbwt-sheep
• @10mg/kg bwt-cattle
• Clorsulon
• @2mg/kgbwt-s/c
• Oxyclozanide
• 12mg/kgbwt

57.  Fascioloides magna:
• Parasite of deer.
• Can also infect grazing animals.
 Dicrocoelium dendriticum:
• IIH:snail-helicella spp
Cercaria passed in slime ball used as food by
ants--grazing animal swallow ant—bile duct.

58.  Seen in all ruminants.
 Etiology:Fusobacterium necrophorum(80-90%).
 Other causes: corynebacterium pyogenes
streptococcus
staphylococcus
bacteriodes.
 Liver is susceptible to abcesses because it recieves blood from
hepatic artery, portal system & umblical vein in fetus & neonates.
 Feed lot cattle mostly affected.

59. Pathopysiology & pathogenesis

60. 1. Abscesses may rupture into vein or form thrombus in caudal
vena cava producing portal hypertension.
hydrostatic pressure & both ascites & diarrhoea can be seen.
2.Emboli from thrombus may be carried to lung.
Hematogenous pneumonia with sepsis & pulmonary
hypertension.
3. Enlarged absecces may obstruct bile duct,excretion of
bilirubin,bile acids & phylloerythrin.

61.  Weight loss.
 Decreased milk production.
 Fever & anorexia.
 Pain on moving ,lying down &
on physical examination.
 CVCT: 3symptoms:-
1. Sudden death from shock.
2. Epistaxis , hemoptysis &
anemia.
3. Severe dyspnea , open
mouth breathing & abnormal
lung sounds.
 Photosensitization & icterus.
 Peritonitis.

62.  Clinical pathology:
• Plasma fibrinogen is activated.
• Total plasma protein is elevated-globulin.
• In CVCT-globulin -9g/dl.
• Decreased PCV,hb,RBC count.
• Liver enzyme-GGT,SDH,AST.
 TREATMENT:
 OTC @ 75mg/head/dat.
 Tylosin @60-90mg/kg/head

63.  FAT COW SYNDROME
 Caused by mobilization of excessive quantities
fat from body depots to liver during period of
negative energy balance at parturient period.
 Cow that become obese before parturation are
more predisposed.
 Morbidity-50-90%.

64.  Fatty acids synthesises in liver & are stored as
triglycerides in extra-hepatic site.
during negative energy balance triglycerides in adipose
tissue are converted to glycerols & NEFA.
albumin bound NEFA acts as source of energy & gets
deposited in liver,spleen,mammary glands,muscles.
liver recieves much of NEFA & due to large blood
supply.

65.  In liver NEFA is back re-esterfied to tryglycerides
& remain in liver until they can be oxidized or
repackaged in envelope of –cholestrol
phospholipids
proteins.
which is very slow proccess leading to fatty liver.
 Increased glucose influences & favoures fatty
liver syndrome & opposite favours ketosis..

66. Clinical signs Clinical pathology & diagnosis
 Depression.
 Anorexia.
 Deblitation.
 Weakness.
 Decreased milk production
 ketonuria.
 Affected cow may show
signs:
 Milk
fever,ketosis,indigestion,LD
A,metritis,mastitis,salmonel
losis.
 Glucose:below 40mg/dl
 Ketone bodies:80-100mg/dl
 FFA: above 7mg/100ml
 OCT:above 200sigma U/ml
 SDH:above 500 sigma U/l
 AST:above 100 units/l
 NEFA:more 1000mEq/l
 Leukopenia denerative left shift
 PCV -.increased
 BUN- increased
 BSP test done

67.  Obesity.
 Large quantity of
omental fat.
 Liver
enlarged,rounded,swo
llen edges,pale
yellow in color,often
floats in water.
 Fatty infilteration of
hepatocytes

68.  Glu ,Ca, Mg salts are given.
 Symptomatic treatment-glucose given.
 Choline chloride(50%)-50g orally once-precursor of
lipoprotein.
 Inositol & methionine also given.
 Insulin @ 200-300IU.s/c twice daily.

69.  Increased NEFA level declines DMI.
 Oxidation of NEFA will lead to formation of ketone bodies.
 Low glucose level-low insulin level(inhibits fat mobilization
from adipose tissue).

70.  PROTEIN ENERGY MALNUTRITION & PREGNANCY
TOXEMIA OF BEEF COWS:
• Usually occuring during winter manifested by
weight loss,weakness, depression & sometime
inability to rise.
• Condition results because of negative energy
balance.

71. DRUGS LESIONS
CCl4 Centrilobular necrosis or fatty
degeneration
hexachlorethane Centrilobular or massive necrosis
alcohol Necrosis-cirrhosis
tetracycline Fatty degeneration
clindamycin Cholestiasis,icterus
erythromycin Cholestasis,icterus
isoniazid Cirrhosis,massive necrosis
rifampin Cholestasis,icterus
Halothane,isoflurane Cirrhosis,massive necrosis
Some diuretic Cholestasis,necrosis
diazepam Cholestasis,icterus
phenobarbital Necrosis/cholestasis,icterus

72. PLANTS LESIONS
LANTANA (Lantana camara) necrosis
RABBIT BRUSH (Tetradymia) necrosis
PANIC GRASS (Panicum spp )
COCKLEBUR (Xanthanium) Haemorrhagic necrosis
LUPIN E(Lupinus spp) Necrosis
COTTONSEED (Gosssypium spp) necrosis+cardiomyopathy
POISONOUS MUSHROOM() Necrosis+ CNS signs
BLUE GREEN ALGAE (microcystis
aeruginosa)
necrosis

73.  Causes secondary photosensitization.
 Plant contains toxin:lantadene A
 lantadene B
 Incidence maximum in summer.
 Clinical signs:
 Constipation
 Ataxia
 Incordination movements
 Photophobic
 Photosenstization-fissures on muzzle,ear tips
 Erythema,odema
 Depressed
 rumenpstasis
 Anorectic
 Jaundice.
 Faeces may contain blood.

74.  Biochemical findings:
 Elevated cojugated bilirubin.
 Necropsy:
 Yellow ,mottled liver
 hepatomegaly
 Treatment:
 Animal should be house fed.
 Laxatives i.e mineral oil.
 Liver tonics.
 Corticosteroids given.
 Secondary skin infection treatment.

75.  Common plants:
1. Senecia lacobaea
2. Senecia vulgaris
3. Senecia longilobus
4. Crotolaria spp.

76.  PA are poisonous plants containing 4-6 different
alkaloids.
after absorbtion via portal cirucaltion carried to liver
Pyrrole cross link with dsDNA.
antimomotic effect
Toxic pyrroles

77.  Hepatocytes become megalocytes*
 also inhibit protein synthesis.
hepatocyte death.
CLINICAL SIGNS:
Diarrhoes
Tenesmus
Prolapsed rectum
ascites

78. Clinical pathology & necropsy
Treatment
 Rise in GGT,ALP.
 Necropsy:
• Hepatic megalocytes.
• Biliary hyperplasia.
• Necrosis
• Fibrosis
• Venoocuslive disease.
 Provide low protein
diet.
 Herbicide spraying.

79. CHEMICAL SOURCE LIVER LESIONS
CCl4 Fumigant,solvent Fatty degeneration
Centrilobular necrosis
Cl-hydrocarbon Insecticide,solvent necrosis
phenol Wood
preservative,disinfectant
Haem centrilobular
necrosis
iron Iron supplements Portal necrosis
copper Toot bath,molluscides, Portal
vaculation+Hemolytic
crisis
phosphorus Fertilizers,rhodenticides Portal necrosis+fatty
degeneration
Tannic acid Skin astrigent Centrilobular necrosis
Paraquat/diquat herbicides Centrilobular necrosis

80. 1. Telangiectasia.
2. Ischemia,hypoxia & cogestion.
3. Fetal liver damage.
4. Neoplasia.
5. Failure of drug metabolism & excretion.
 Other:
1. Cholelithiasis.
2. Cholangitis.
3. Cholecystitis.

81. TELANGIECTASIA (SAW DUST):
•Its focal degeneration in liver lobular circulation chr by red- brown
foci (1-5mm in dia).
• Hepatocytes are distorted & sinusoids are congested.
ISCHEMIA,HYPOXIA & CONGESTION:
•Can lead to death of hepatocytes.
•Chronic passive congestion causes grossly visible nutmeg liver.
FETAL LIVER DAMAGE:
•Damaged by infectious & toxic agents
•Aborted fetus of cattle-IBR.

82. FAILURE OF DRUG METABOLISM & EXCRETION:
•Delayed clearance with hepatic insufficiency.
•Chloremphenicol,tetracycline,erythromycin.

83. CHOLELITHIASIS
• Presence of
calculi in gall
bladder or
common bile
duct.
• Observed in
cattle.
• Ca, bile salts,
cholestrol etc.
CHOLANGITIS
• Inflammation of
biliary duct system.
• In cattle liver
flukes due to
irritation & toxins.
• Decreased milk
production,
hypophagia,
tachycardia,anorexi
a,diarrhoea.
CHOLECYSTITIS
• Inflammation of
gall bladder.
• Bacterial
infection with E
coli,
salmonella,are
observed.

84. sumreen2707@gmail.com