Lecture 13 2/11/25 Flashcards

1
Q

What are the characteristics of canine chronic hepatitis?

A

-inflammatory reaction in the liv3er continuing without improvement for 6+ months
-confirmed via histology
-most common primary liver dz in dogs
-often idiopathic
-higher prevalence of chronic bacterial infections in dogs with CCH

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2
Q

What are possible etiologies for CCH?

A

-infection
-medications
-toxins
-drug-induced chronic hepatitis
-excess hepatic copper accumulation
-autoimmune chronic hepatitis

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3
Q

What is the most common cause of toxin-induced CCH?

A

copper accumulation

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4
Q

What is the pathophysiology of CCH?

A

-hepatic injury results from hepatocellular death and release of inflammatory mediators
-inflammatory cell infiltration and immune system response contributes to ongoing injury
-ongoing injury eventually leads to necrosis and fibrosis

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5
Q

What is the signalment of CCH?

A

-seen in middle-aged to older dogs
-can be any breed, but some are predisposed

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6
Q

Why do signs of CCH not show up until late in the disease process?

A

the liver has a large reserve capacity and can continue functioning normally early in disease

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7
Q

Why is it important to test dogs with persistent increases of liver enzymes early?

A

waiting for clinical signs means the patient will lose a lot of functional liver capacity; early diagnosis can lead to earlier treatment and preservation of function

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8
Q

What are the less specific clinical signs seen in CCH patients?

A

-fever
-lethargy
-weakness
-hyporexia/anorexia
-weight loss
-abdominal pain
-vomiting diarrhea

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9
Q

What are the more specific clinical signs seen in CCH patients?

A

-PU/PD
-icterus
-ascites
-hepatic encephalopathy

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10
Q

What are the characteristics of liver enzyme clin path in CCH?

A

-liver enzymes are increased in a mixed hepatocellular and cholestatic pattern
-initial increase in leakage enzymes; ALT and AST
-cholestatic enzymes increase later
-enzymes can wax and wane over the course of months

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11
Q

What causes abnormal markers of hepatic synthetic function in CCH?

A

-hepatocyte loss
-fibrosis limiting normal sinusoidal blood flow

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12
Q

What are the characteristics of ultrasound as a diagnostic tool for CCH?

A

-not sensitive or specific for the diagnosis of CCH
-may see. small, hyperechoic liver
-helpful to identify neoplastic masses, ascites, and APSS

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13
Q

What are the characteristics of hepatic cytology as a diagnostic tool for CCH?

A

-inadequate for diagnosis of CCH
-can help to rule out diffuse neoplastic infiltration and suppurative inflammation

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14
Q

What tests need to be done to diagnose CCH?

A

-histology
-aerobic/anaerobic culture
-copper quantification

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15
Q

What are the histologic features of CCH?

A

-inflammation in any region of the liver
-hepatocellular death
-variable grades of fibrosis

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16
Q

What are the main management steps for CCH?

A

-discontinue hepatotoxic drugs
-treat underlying disease; may be enough to stop progression
-antioxidant therapy to control necroinflammatory/cholestatic processes until liver enzymes normalize

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17
Q

What are further recommendations for treatment of CCH?

A

-antiemetics and gastroprotectants
-antibiotics if bact. infection is suspected
-treatment for fibrosis if present on histology
-protein restriction ONLY if patient develops acquired stunts or hepatic encephalopathy

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18
Q

What are the specific management steps for copper-associated chronic hepatitis?

A

-lifelong dietary restriction; commercial liver diet + low-copper protein source supplementation
-chelation of copper if concentrations reach 750 ug/g of centrilobular accumulation or 1500 ug/g overall accumulation

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19
Q

What are the characteristics of D-penicillamine?

A

-bind hepatic copper for elimination in urine
-upregulate metallothionein in enterocytes for fecal elimination of dietary copper
-has anti-inflammatory and anti-fibrotic properties

20
Q

How long should D-pen be used?

A

-6 to 9 months until copper concentrations normalize when combined with a copper-restricted diet
-longer if not given with a copper-restricted diet

21
Q

How is the efficacy of copper hepatitis determined?

A

-repeat biopsy and quantification is best
-normalization of serum ALT is a good surrogate

22
Q

Which treatments can be used for maintenance of copper hepatitis?

A

-D-pen given at a reduced frequency
-administration of zinc to block enteric copper absorption
-D-pen and zinc CANNOT be given concurrently

23
Q

What are the options for immune modulation in nonsuppurative immune-mediated CCH?

A

-prednisone/prednisolone
-dexamethasone if ascites occurs
-steroids combined with secondary immunosuppressive med.
-cyclosporine alone
**often lifelong therapy

24
Q

What is the prognosis of CCH?

A

-depends on etiology and histologic grade
-infectious and copper-associated hepatopathy have good prognosis
-fibrosis could be reversible; therapy indicated even in severe fibrosis
-ascites and icterus are negative prognostic indicators in dogs with idiopathic CCH

25
Q

What is canine vacuolar hepatopathy?

A

excessive accumulation of cytosolic glycogen, fat, and water within hepatocytes

26
Q

What is the predominant etiology for canine vacuolar hepatopathy?

A

secondary to disease in other organs

27
Q

What are the characteristics of glycogen-like vacuolar hepatopathy of scottish terriers?

A

correlated to abnormal androgenic hormone production

28
Q

What are the characteristics of canine familial hyperlipidemia?

A

-occurs in miniature schnauzers
-canine primary hepatic steatosis (excessive fat in liver)
-caused by delayed clearance of dietary triglycerides
-causes increases in fasting triglycerides and/or cholesterol

29
Q

What is the pathophysiology of vacuolar hepatopathies?

A

-dysregulation in the synthesis, storage, and catabolism of glycogen leads to hepatocellular swelling and dysfunction
-failure to address underlying dz allows hepatocellular swelling to affect normal intracellular processes
-hepatocellular swelling also affects extracellular canalicular bile flow
-continued cellular degeneration leads to stromal collapse and distortion of sinusoidal blood flow

30
Q

What is the clinical presentation of vacuolar hepatopathies?

A

-middle-aged to older dogs
-any breed or gender
-hepatomegaly on physical exam
-moderate to severe increase in ALP and ALT
-progressive increase in leakage enzymes with ongoing hepatocellular damage

31
Q

What are the differential diagnoses for vacuolar hepatopathies?

A

-primary or secondary cholestatic liver dz
-neoplasia

32
Q

What are indicators for preliminary diagnosis of vacuolar hepatopathy?

A

-moderate to severe ALP increase
-hepatomegaly
-hyperechoic parenchyma with hypoechoic nodules
-decreased density of hepatocytes on cytology

33
Q

Why is histology needed in vacuolar hepatopathy diagnosis?

A

to diagnose concurrent necroinflammatory dz

34
Q

What are the management steps for vacuolar hepatopathy?

A

-therapy of underlying condition
-discontinuation of glucocorticoids, steroidogenic drugs, and herbal remedies
-antioxidant therapy
-low fat diet for hyperlipidemia
–omega-3 fatty acids if low fat diet fails

35
Q

What is the prognosis for vacuolar hepatopathy?

A

-good if underlying etiology is identified and treated
-can see a progressive degenerative process correlated w/ development of hepatocellular carcinoma

36
Q

What are the characteristics of gallbladder mucocele?

A

-abnormal accumulation of mucin and inspissated bile within gallbladder lumen
-specific etiology unknown

37
Q

Which co-morbidities are associated with gallbladder mucocele?

A

-dyslipidemia
-endocrinopathy
-gallbladder hypomotility
-cholelithiasis

38
Q

What is the pathophysiology of gallbladder mucocele?

A

-excessive secretion of abnormal gel-forming mucin from gallbladder epithelium leads to gallbladder distension and mural ischemia/necrosis
-obstruction of the cystic and common bile ducts occurs secondary to extension or migration of mucin

39
Q

What is the clinical presentation of gallbladder mucocele?

A

-older, small to mid-sized dogs
-may be asymptomatic
-GI signs, cranial abdominal pain, and icterus
-predominating increase in cholestatic enzymes (ALP, GGT)
-increase in leakage enzymes (ALT, AST
-variable changes in WBC, bilirubin, and cholesterol

40
Q

What are the differential diagnoses for gallbladder mucocele?

A

-cholecystitis
-hemocholecyst
-accumulation of gravity-independent gallbladder sludge due to outflow obstruction

41
Q

How is gallbladder mucocele diagnosed?

A

abdominal ultrasound

42
Q

When is cholecystectomy indicated?

A

-ruptured gallbladder mucoceles
-symptomatic patients
-those with moderate/severe biochemical changes

43
Q

What are the characteristics of cholecystectomty?

A

-bacterial cholecystitis is a common co-morbidity
-broad-spectrum ABs should be given to decrease complications from septic peritonitis
-vitamin K1 given peri-operatively
-choleretics should not be given if GB wall is compromised or if bile duct is obstructed

44
Q

What are the medical management steps for gallbladder mucoceles in asymptomatic/minimally affected patients?

A

-ursodeoxycholic acid
-therapy of underlying dyslipidemias/endocrinopathies
-serial rechecks; cholecystectomy if no improvement

45
Q

What is the prognosis for gallbladder mucoceles?

A

-post-op survival is relatively high
-survival is better in patients undergoing elective surgery
-hyperbilirubinemia is a poor prognostic indicator