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SAM Final > 23. Chronic hepatitis, familiar liver diseases in dogs > Flashcards

23. Chronic hepatitis, familiar liver diseases in dogs Flashcards

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

A

Periportal

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
Q

treatment of CUCH

A

Chelating drugs actively bind to extracellular copper

26
Q

Copper storage disease in Bedlington terrier

A

progressive accumulation of copper resulting from failure of normal hepatic biliary excretion

27
Q

3 forms of homozygous genotype of Copper storage disease in Bedlington terrier

A

Asymptomatic form
Acute form
Chronic form

28
Q

Asymptomatic form of homozygous genotype of Copper storage disease in Bedlington terrier

A

Only affects young animals
copper in lysosomes
increased ALT
No structural damage

29
Q

Acute form of homozygous genotype of Copper storage disease in Bedlington terrier

A

Young adults
Rare
lethargy
vomiting
depression
anorexia
death within 2-3 days

30
Q

Chronic form of homozygous genotype of Copper storage disease in Bedlington terrier

A

Young/ middle aged
Focal random hepatic necrosis
increased ALT

31
Q

heterozygous genotype of Copper storage disease in Bedlington terrier

A

transient increase in copper

32
Q

autosomal recessive genotype of Copper storage disease in Bedlington terrier

A

remove from breeding

33
Q

Copper storage of dobermanns

A

2 types of chronic hepatitis
Primary Cu toxicosis and CuCH
develop it at a much lower level than in bedlingtons

34
Q

Treatment of abnormal copper storage diseases

A

Copper chelators
D - penicillamine
Zn salt
Antioxidants - SAMe, Vit E, Silymarin

35
Q

D- penicillamine drug

A

not to be used with Zn
decreased copper in liver
increase liver metallothionine

36
Q

Zn salts drugs

A

dont use with chelators or d- penicillamine
decrease intestinal absoprtion of copper
good in case of cholestasis

37
Q

what are the normal leverls of copper

A

<400 ug/ g

38
Q

Lobular Dissecting Hepatitis

A

thought to be a response of the liver to insults at juvenile age

39
Q

Consequences of Lobular Dissecting Hepatitis

A

Portal hypertension –> ascites, APSS
Lymphocytes, plasma cells scattered throughout hepatic lobule
Bands of collagen and reticulin fibres around hepatocytes

40
Q

cause of Non specific reactive hepatitis

A

consequence of extrahepatic diseases
metabolic - cushings, DM, hyper/ o thryoidism
IBD, PLE
Pancreatitis, sepsis, IHA, FIP, toxoplasma

41
Q

Clinical signs of Non specific reactive hepatitis

A

increased; AKT, AKP
Hypoxia
Anorexia
No nerosis

42
Q

cause of Nodular Hyperplasia

43
Q

predisposition to Nodular Hyperplasia

A

older dogs
usually seen PM

44
Q

Lab D of Nodular Hyperplasia

A

Increased ; alp, alt

45
Q

Histopath of Nodular Hyperplasia

A

vacuolised hepatocytes
Normal lobular structure
no fibrosis, necrosis, inflammation

46
Q

Treatment of chronic hepatopathies

A

Prednisolone
Immunosuppressants
Choleretic
Antifibrotic
Antioxidants

47
Q

Prednisolone in chronic hepatopathies

A

Immunosuppressive dose
Improvement of necrotic inflammation and coagulopathy
decreases inflammation

48
Q

other immunosuppressants in chronic hepatopathies

A

cortico steroids
dex
cyclosporine
azathioprine

49
Q

Choleretics for chronic hepatopathies

A

UDCA
hepatoprotective, anti inflam, anti fibrotic
Helps elimination of toxin

50
Q

Antifibrotics for chronic hepatopathies

A

colchicine
prednisolone
D - penicillamine
vit e
UDCA

SAM Final (48 decks)

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