HEPATITIS PPT.pptx WITH GOOD EXPLANATION OF CHRONIC AS WELL AS ACUTE

Ashishkumar1790963 206 views 15 slides Apr 28, 2024
Slide 1
Slide 1 of 15
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15

About This Presentation

GOOD INFORMATION


Slide Content

HEPATITIS Hepatitis is inflammation of the liver. Hepatitis can be caused by, several viruses (viral hepatitis), chemicals,drugs , certain genetic disorders an overactive immune system that attacks the liver, called autoimmune hepatitis. hepatitis can be acute, which flares up suddenly and chronic, which is a long-term condition usually producing more subtle symptoms

ACUTE HEPATITIS Acute hepatitis can be caused by Drugs ( antibiotic nalidixine acid), Viral infection (infectious canine hepatitis), Mycotoxins (especially aflatoxin B1). Hepatitis resulting from sepsis (reactive hepatitis), Leptospirosis Toxins (Mushroom toxicity dose dependent toxicity like acetaminophen toxicity in dog and cat)

Pathogenesis Acute hepatitis is characterized by, liver necrosis and the inflammation. Necrosis is a liquefying necrosis collapse of the reticular framework. There are also ceroid-filled macrophages called “scavenger cells”. Infection with canine adenovirus-1 Characterized by confluent and bridging necrosis in the centrilobular zone and by the presence of intranuclear inclusions in hepatocytes and Kupffer’s cells.

Symptom Acute illness, Sometimes fever, Anorexia,Vomiting , Dehydration, Sometimes icterus, Tendency for bleeding. Diagnosis- Blood examination: Elevation of liver enzymes, especially ALT.(SGPT) Diagnosis is confirmed by liver biopsy Hepatic encephalopathy in fulminant hepatitis (massive necrosis of liver parenchyma) is characterized by high blood NH 3  values.

Management and Treatment Symptomatic treatment is possible: iv fluid to correct hypovolemia, shock, acidosis or alkalosis, hypoglycaemia, and electrolyte disturbances. Avoid corticosteroids; in acute infections they are contraindicated. acetaminophen intoxication cause oxidative damage should be treated with silymarin (50 mg/kg/day) for 3–5 days.

Acetaminophen intoxication may also be treated with the combination of N- acetylcysteine (140mg/kg PO, every six hours during three days), Vitamin C (25–35 mg/kg PO, every six hours for two days), and cimetidine 5 mg/kg/bid for 4 days. Dogs with acetaminophen intoxication may have hemolysis and blood transfusion may be required.

CHRONIC HEPATITIS Chronic hepatitis is characterized by, Periportal fibrosis, infiltration of lymphocytes and plasma cells, periportal liver cell apoptosis or necrosis. Apoptotic liver cells become smaller and acidophilic; they are known as acidophilic bodies. Limiting plate, which is the layer of cells dividing the portal tracts from the liver parenchyma, may become disrupted with expansion of the inflammatory reaction from portal areas into the parenchyma. This invasion may extend to form porto -portal or porto -central bridging fibrosis.

Etiology Chronic hepatitis may be the result of a viral infection. The common canine adenovirus-1 (CAV1) of infectious canine hepatitis is the only known canine hepatitis virus. CAV1 virus infection in non-vaccinated animals gives fulminant hepatitis. Lymphocytic and plasmacellular inflammation, and the good response to immune suppressive drugs indicate that a self-perpetuating autoimmune type of liver cell necrosis causes the chronic progression.

Fibrosis, especially in cased of cirrhosis, obstructs the normal blood flow to the liver, which primarily affects the low pressure portal blood supply. Portal blood is required to activate local growth factors in the liver, so that decreased portal perfusion also contributes to decreased liver regeneration. Chronic hepatitis and cirrhosis are associated with variable degrees of intrahepatic cholestasis,

Pathogenesis Chronic hepatitis may be a chronic extension of acute hepatitis, Gradually progressive liver cell necrosis may cause elevation of all liver enzymes and the bile acids. Liver function is diminished by the loss of functional tissue and reduced portal blood flow. low albumin and fibrinogen levels. Conversion of ammonia remains adequate until portosystemic collaterals develop.

Hepatic encephalopathy may develop if portosystemic collaterals are formed. Hypoalbuminemia and portal hypertension may cause ascites (transudate). In breeds in which an abnormal copper metabolism causes hepatitis, the gradual accumulation of copper usually leads to clinical signs at an age of 4–6 years. Most frequently affected breeds are Labrador retrievers Dobermann Pinschers, all spaniel breeds,

Clinical sign- Abdominal distension, Vomiting, Diarrhoea, Hepatoencephalopathy , Jaundice, Lethargy, Polydipsia/polyuria, Weigth loss

Physical examination finding Ascites Abnormal mucus membrane colour Abnormal capillary refill time Icterus Diagnosis:- Made by liver biopsy. Ultrasonography prior to biopsy is advised; Cirrhosis may be suspected by the appearance of a small liver with an irregular surface and structure.

Treatment and Management If ascitis is is causes respiratory problem then drainage of peritoneal fluid required Predinisolon @1-2mg/kg bdwt I/m For 2-3weeks then slowly tapper to Lower effective dose as a antifibrotic antiinflammatory,immunosuppressive Omeprazole@1-2mg /kg iv as a antacid Silymarin / silybinin @20-50mg /kg bdwt po as antioxidant A broad spectrum antibiotics

THANK YOU
Tags