23. Chronic hepatitis, familiar liver diseases in dogs Flashcards

(50 cards)

1
Q

chronic heapatopathy in general

A

toxins; drugs —> chronic liver failure –> end stage liver

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2
Q

liver fibrosis definition

A

reversible
non regenerative nodule

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3
Q

Liver cirrhosis definition

A

irreversible
fibrosis and regenerative nodules

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4
Q

Clinical signs of chronic hepatopathy

A

anorexia
weight loss
ascites
PU/PD
Icterus
coagulopathy
CNS signs

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5
Q

Lab D of chronic hepatopathy

A

Increased ; ALT, ALP, BA, NH3
Decreased ; Albumin, BUN, microcyctosis

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6
Q

Biopsy of chronic hepatopathy

A

Piecemeal Necrosis
Bridging Necrosis
Chronic Active hepatitis
Lobular dissecting hepatitis

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7
Q

What is piecemeal necrosis

A

necrosis of hepatocyte layer adjacent to portal tract

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8
Q

What is bridging necrosis

A

tracts of necrosis across the hepatic lobule from portal areas –> central veins

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9
Q

What is chronic active hepatitis

A

Periportal inflammation
& piecemeal necrosis

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10
Q

What is lobular dissecting hepatitis

A

Lobular hepatitis associated with dissecting tracts of fibrosis

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11
Q

what characterises chronic hepatitis

A

mononuclear/ mixed infiltrate in the liver with accompanied periportal necrosis & fibrosis

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12
Q

what can chronic hepatitis lead to

A

hepatic cirrhosis

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13
Q

Predisposition to chronic hepatitis

A

bedlington terrier
doberman
westies
cocker
dalmatian
poodle
lab

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14
Q

Pathophys of chronic hepatitis

A

poorly understood

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15
Q

causes of chronic hepatitis

A

toxins / drugs
copper
infectious agents - lepto, helicobacter
Immune mediated
idiopathic

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16
Q

clinical signs of chronic hepatitis

A

anorexia
weight loss
vomiting
weakness
mild gi signs
PU/ PD
ascites
jaundice
depression

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17
Q

Lab d of chronic hepatitis

A

increased ; ALP. ALP. BA. Br
Decreased ; albumin
Non regen anaemia

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18
Q

Diagnosis of chronic hepatitis

A

Biopsy - definitvie diagnosis
US - nodular in cirrhosis

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19
Q

Treatment of chronic hepatitis

A

immunosuppression
Avoid corticosteroids
Treat underlying cause

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20
Q

location of primary Copper- caused chronic hepatitis (CUCH)

A

centrilobular

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21
Q

location of secondary CUCH

22
Q

where is copper stored

A

stored and encapsulated in hepatocyte lysosomes
therefore inaccessible by chelating drugs

23
Q

when does CUCH become clinically significant

A

Rupture of lysosomes –> free IC copper —> necrosis
when copper > 2000ppm

24
Q

diagnosis of CUCH

A

histology
histochem copper staining

25
treatment of CUCH
Chelating drugs actively bind to extracellular copper
26
Copper storage disease in Bedlington terrier
progressive accumulation of copper resulting from failure of normal hepatic biliary excretion
27
3 forms of homozygous genotype of Copper storage disease in Bedlington terrier
Asymptomatic form Acute form Chronic form
28
Asymptomatic form of homozygous genotype of Copper storage disease in Bedlington terrier
Only affects young animals copper in lysosomes increased ALT No structural damage
29
Acute form of homozygous genotype of Copper storage disease in Bedlington terrier
Young adults Rare lethargy vomiting depression anorexia death within 2-3 days
30
Chronic form of homozygous genotype of Copper storage disease in Bedlington terrier
Young/ middle aged Focal random hepatic necrosis increased ALT
31
heterozygous genotype of Copper storage disease in Bedlington terrier
transient increase in copper
32
autosomal recessive genotype of Copper storage disease in Bedlington terrier
remove from breeding
33
Copper storage of dobermanns
2 types of chronic hepatitis Primary Cu toxicosis and CuCH develop it at a much lower level than in bedlingtons
34
Treatment of abnormal copper storage diseases
Copper chelators D - penicillamine Zn salt Antioxidants - SAMe, Vit E, Silymarin
35
D- penicillamine drug
not to be used with Zn decreased copper in liver increase liver metallothionine
36
Zn salts drugs
dont use with chelators or d- penicillamine decrease intestinal absoprtion of copper good in case of cholestasis
37
what are the normal leverls of copper
<400 ug/ g
38
Lobular Dissecting Hepatitis
thought to be a response of the liver to insults at juvenile age
39
Consequences of Lobular Dissecting Hepatitis
Portal hypertension --> ascites, APSS Lymphocytes, plasma cells scattered throughout hepatic lobule Bands of collagen and reticulin fibres around hepatocytes
40
cause of Non specific reactive hepatitis
consequence of extrahepatic diseases metabolic - cushings, DM, hyper/ o thryoidism IBD, PLE Pancreatitis, sepsis, IHA, FIP, toxoplasma
41
Clinical signs of Non specific reactive hepatitis
increased; AKT, AKP Hypoxia Anorexia No nerosis
42
cause of Nodular Hyperplasia
unknown
43
predisposition to Nodular Hyperplasia
older dogs usually seen PM
44
Lab D of Nodular Hyperplasia
Increased ; alp, alt
45
Histopath of Nodular Hyperplasia
vacuolised hepatocytes Normal lobular structure no fibrosis, necrosis, inflammation
46
Treatment of chronic hepatopathies
Prednisolone Immunosuppressants Choleretic Antifibrotic Antioxidants
47
Prednisolone in chronic hepatopathies
Immunosuppressive dose Improvement of necrotic inflammation and coagulopathy decreases inflammation
48
other immunosuppressants in chronic hepatopathies
cortico steroids dex cyclosporine azathioprine
49
Choleretics for chronic hepatopathies
UDCA hepatoprotective, anti inflam, anti fibrotic Helps elimination of toxin
50
Antifibrotics for chronic hepatopathies
colchicine prednisolone D - penicillamine vit e UDCA