7. In toxic hepatitis, the usual lesion is
centrilobular and varies from
cloudy swelling to acute necrosis
with a terminal vena-occlusive
lesion in some plant poisonings.
8. In infectious hepatitis, the lesions
vary from necrosis of isolated cells
to diffuse necrosis affecting all or
most of the hepatic parenchyma.
9. In parasitic hepatitis, the changes
depend upon the number and type
of migrating parasites. In massive
fluke infestations sufficient damage
may occur to cause acute hepatic
insufficiency
10. Nutritional hepatitis is characterized by
massive or submassive necrosis. Hepatic
lipidosis is characterized by fatty
infiltration of hepatocytes progressing
to development of fatty cysts.
11. Congestive hepatitis is characterized
by dilatation of central veins and
sinusoids with compression of the
parenchymal cells.
14. 4. Constipation and punctuated by
attacks of diarrhoea.
5. Oedema and emaciation.
6. Bleeding tendency due to clotting
deficiency.
15. 7. The nervous signs vary from ataxia
and lethargy with yawning, or
coma, to hyperexcitability with
muscle tremor, mania, including
aggressive behavior, and
convulsions.
16. A characteristic syndrome is the
dummy syndrome, in which
affected animals push with the
head, do not respond to normal
stimuli.
17.
18. 8. Subacute abdominal pain, usually
manifested by arching of the back,
and pain on palpation of the liver.
20. 10. Photosensitization in animals fed on
green fodders and exposed to
sunlight.
Fig. Photosensitized animal
21. 11. In chronic hepatitis, the signs
developed slowly and persist for a
longer periods.
12. Ascites and dummy syndrome are
more common in chronic than acute
form.
22. Clinical signs.
Liver function tests: Estimation of serum
total, direct and indirect bilirobin. In
addition to AST, ALT, ALP, LDH, SD,
Albumin.
Biopsy of Liver.
Sonography of Liver.
23. Encephalopathy:
Hepatitis is easily misdiagnosed as
an encephalopathy unless jaundice
or photosensitization is present.
Acidosis:
By History and Clinical examination.
24. Give diet high in CHO, Ca++, and low in
protein and fat.
Purgation and enemas have also
been used but mild purgation is
recommended.
Injection of glucose (25 or 40%) and
Vitamins.
25. Specific antimicrobial drugs.
Hepatic fibrosis is considered to be a
final stage in hepatitis and treatment
is not usually undertaken.
Editor's Notes
Hepatic injury caused by nutritional deficiency.Increased pressure in the sinusoids of the liver causes anoxia and compression of surrounding hepatic parenchyma. Congestive heart failure is the common cause and leads to centrilobular degeneration.Serum hepatitis in the horse is characterized by severe central lobular necrosis following the administration of biologics of equine origin such as tetanus antitoxin, commercial equine plasma.
The cardinal signs of hepatitis are anorexia, mental depression - with excitement in some cases, muscular weakness, jaundice and in the terminal stages somnolence, recumbency and coma with intermittent convulsion.
Ventral Oedema due to hepatic failure (hypoproteinaemia).
The liver is unable to excrete a metabolite of chlorophyll from forages the animal has eaten. The metabolite accumulates in the skin and is activated by sunlight. The reaction yields free radicals that "burn" the epidermis. Affected skin becomes wrinkled, and the surface may eventually slough away. Recovery may take weeks. Scarring may be obvious after healing occurs. Areas most affected include lightly or unpigmented skin.
Acute diseases affecting the alimentary tract, particularly engorgement on grain in cattle and horses; may be manifested by signs of nervous derangement resembling those of acute hepatic dysfunction but the history and clinical examination usually suggest a primary involvement with the alimentary tract.
CHO for Ascites and Oedema.Protein may lead to NH3 intoxication.mild purgation is recommended to avoid unnecessary fluid loss.
