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sam dr green > caninehepatobiliary > Flashcards

caninehepatobiliary Flashcards

1
Q

in dogs this 2 cs are nt predictable PRESENT in hepatobiliary dz

A

Jaundice & hepatomegaly

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2
Q

Hepatic failure” more common in dog

A
  • Abdominal effusion
  • Acquired PSS
  • Portal hypertension
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3
Q

characteristics of CHRONIC HEPATITIS

A
  • Comprises a broad spectrum of diseases
  • Often have similar:
    • History (sick for weeks –months)
    • Clinical findings
    • Histopathology findings
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4
Q

SIGNALMENT FOR CHRONIC HEPATITIS

A

Generally middle-aged dogs

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5
Q

HALLMARK FOR CHRONIC HEPATITS

A
  • Elevated ALT early in disease (animals often not sick)
  • Followed by loss of hepatic function late in disease
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6
Q

ETIOLOGY FOR CHRONIC HEPATITIS

A

Multiple etiologies, often idiopathic

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7
Q

DEFINITIVE DX FOR CHR. HEPATITIS

A

Liver biopsy required for diagnosis & prognosis

N.B TRUE CUT NT ENOUGH IN DOGS

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8
Q

COMMON FEATURES OF CHR. HEPATITS ON HISTOPATHOLOGY

A
  • Hepatocellular necrosis
  • Inflammatory cell infiltrates
  • Fibrosis
  • Biliary hyperplasia
  • Nodular regeneration
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9
Q

COMMON GOAL FOR CHRNIC HEPATITIS TX

A
  • Reverse or control inflammatory process
  • Prevent further fibrosis,
  • treat underlying etiology
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10
Q

CLASSIFICATIONS FOR CH. HEPATITS

A
  • Familial chronic hepatitis
  • Drug administration
  • Infectious agents
    • SUPER UNCOMMON
  • Idiopathic chronic hepatitis
  • Copper -associated chronic hepatitis
    • WHEN TAKING BX ALSO MEASURE CU
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11
Q

DISCUSS MECHANISM FOR FAMILIAL CHRONIC HEPATITIS IN Bedlington Terriers

A
  • Autosomal recessive trait
    • Metabolic error resulting in copper accumulation
    • Hepatocellular disease
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12
Q

HOW DO U DX FAMILIAL CU DZ IN BEDLINTON TERRIERS

A
  • Liver biopsy,
  • LOOK FOR quantitative copper levels for diagnosis
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13
Q

LESIONS FOR FAMILIAL CU DZ IN BEDLINTON TERRIERS

A

Results in hepatitis, cirrhosis

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14
Q

TX FOR BEDLINTON FAMILIAL CU DZ

A
  • copper chelation
    • D-penicillamine (Cuprimine)–CAN HAV GI SIDE EFECTS
    • Trientine
    • Both promote urinary excretion of copper
    • RESTRICITING CU CAN ALSO BE HELPFUL
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15
Q

CAUSE OF CHR. HEPATITIS IN DOBERMAN PINCHERS

A
  • UNKNOWN
  • Familial basis strongly suspected
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16
Q

SIGNALMENT FOR CLINICAL HEPATITIS IN DOBERMANS

A

Most common in females aged 5-7 years of age

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17
Q

WHAT KIND OF HEPATITIS DO DOBERMANS GET

A
  • Copper storage disease, hepatocellular disease
  • DOBIES ARE AFFECTED BY LOW CU LEVELS
  • THAN BELLINGTONS
  • THEY ARE MOST SENSITIVE
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18
Q

WHAT SPECIAL ABOUT WHITE HIGHLANDER TERRIER HEPATITIS

A
  • THEY GET Copper associated hepatopathy
  • Liver copper Does NOT progressively increase with age
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19
Q

LIST THE DRUGS THAT CAUSES CHR. HEPATITS

A
  • Anticonvulsants
  • Glucocorticoids
  • Sulfa drugs
  • Chemotherapeutic drugs
  • N.B phenylbarbitol is the 1 we worry most about
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20
Q

common causes of infectious chrnic hepatitis

A
  • Infectious organisms NOTa common cause of chronic hepatitis
  • Infectious Canine Hepatitis (CAV-1)
    • Canine adenovirus type 1 (CAV-1)
  • lepto usually cause acute hepatitis
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21
Q

most common cause of chr. hepatitis

A

idiopathic chr. hepatitis

mixed breeds

pure breed dogs

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22
Q

tx for chr. hepatits

A
  • Remove the primary etiology
  • Most other therapies are unproven
  • Some therapies controversial
  • Prevention and treatment of excess copper
  • Anti-inflammatory medications
    • steroids will increase ALT and alp
  • Anti-fibrotic agents
    • no evidence it works
  • Dietary modification
    • best way by limiting in diet
  • Hepatoprotectants
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23
Q

how do we reduce cu absoption in gi

A

Zinc (2-3 mg/kg PO q 12h on empty stomach)
Zn –stimulates formation of metallothionein
Swallowed copper binds to this protein
Reduces absorption
Vomiting can be side effect of medication
Bedlingtons (early in life), Westies

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24
Q

most effective method to reduce copper

A
  • Copper chelation

Most effective method to reduce copper

  • D-Penicillamine
    • Cuprimine
    • Antifibrotic, anti-inflammatory properties
  • Trientine
  • Must be given long term for any potential benefit
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25
Q

discuss efficacy of anti-fibrotic medications in chr. hepatitis

A

Colchicine
Inhibits collagen synthesis
Enhances collagenase activity
Not well studied in the dog

Must be given long term for any potential benefit

n.b may prevent future fibrosis

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26
Q

discuss goals of dietary modification in chr. hepatits therapy

A
  • Provide sufficient nutritional support
  • Minimizing effects of hepatic encephalopathy
  • Highly digestible
  • High quality protein in restricted quantities
  • Non-protein sources for majority of calories
  • Notalways required as part of treatment plan
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27
Q

list the hepatoprotectants that may be used in chr. hepatitis

A
  • vit e
    • hepatoproctactant, antioxidative
  • S-adenosyl methionine (SAMe, Denosyl)
    • Hepatoprotectant, glutathione source
  • Ursodiol (Actigall)
    • has antiinflamatory effects
  • Milk thistle?
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28
Q

px for chronic hepatitis

A
  • Advanced chronic hepatitis, cirrhosis –guarded
  • If diagnosed and treated early in disease
    • Mean survival 6 -16 months (one study)
    • Mean survival 20 -30 months (another study)
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29
Q

Poor prognostic indicators for chronic hepatits

A
  • Hypoalbuminemia, hypoglycemia, coagulopathies
  • Cirrhosis (survival < 1 month in one study)
30
Q

how do dogs present with congenital portosystemic shunts

A
  • Presentation similar to cats
  • may be presenting with neurological signs,
  • urinary signs
    smaller than other litter mates
31
Q

signalment for portosystemic shunts in dogs

A
  • Small breed dogs most commonly affected
    • Yorkshire Terrier
32
Q

what type of portosystemic shunt occurs in large breed dogs

A

intrahepatic shunt

33
Q

what type of portosystemic shunt occurs in small breed dogs

A

Single extrahepatic shunts

34
Q

what kind of shunt do cats get

A

single extra hepatic shunt

35
Q

dx,tx and px for portosystemic shunts in dogs

possible complications

A
  • tx similiar to cats
  • Prognosis better for dogs compared to cats
  • Complications of portal hypertension and post operative seizures still possible
  • Important to stabilize PRIORto surgery
  • Treat for hepatic encephalopathy
  • Seizure control
36
Q

definition for microvascular dysplasia

A
  • Clinical features of PSS with no vascular anomaly
    • Normal imaging (u/s,portogram, scintigraphy)
    • Microscopic vascular anomaly
37
Q

signalment for microvascular dysplasia

A

Same breeds affected with PSS

38
Q

tx for microvascular dysplasia

A

No surgical treatment
Treat only if and when signs of hepatic encephalopathy occur

39
Q

how common are primary biliary dz in dogs

A
  • Rare in dog
  • More common in cat
40
Q

causes of secondary biliary dz in dogs

A
  • Pancreatitis (common cause)
  • Sepsis (from non hepatobiliary disease)
41
Q

More common biliary tract disorders

A
  • Extrahepatic bile duct obstruction (EBDO)
  • Bile peritonitis
  • Gallbladder mucocele
  • All require surgical intervention
42
Q

clinical features of biliary tract disorders

A
  • Icterus
  • Acute / chronic vomiting
  • Anorexia, depression, weight loss
  • +/-abdominal pain
43
Q

dx for biliary tract disorders

A
  • Bloodwork –increases in
    • ▪Bilirubin
    • ▪ALP, GGT
    • ▪ALT (less severe)
  • Cholestatic process
44
Q

what can u see on rads with biliary disorders

A
  • Pancreatitis
    • Loss of serosal detain in cranial abdomen
    • Lateral displacement of duodenum
  • Cholelithiasis
  • Limitations?
45
Q

when is US useful in biliary dz dx

A

Differentiate hepatic vs. post hepatic icterus
Is it a surgical case?

Yellow animal with no anemia –ULTRASOUND!

46
Q

can u use Serial bilirubin levels to determine if surgical case?

A

no

47
Q

tx for non obstructive biliary dz

A
  • Supportive care
  • Antibiotics, vitamin K PRN
48
Q

tx for obstructive biliary disorders

A

Surgery (biliary reconstruction PRN)
Biopsy
Culture

49
Q

Inflammation of bile ducts

A

uncommon

cholangitis

50
Q

Inflammation of gallbladder

A

Cholecystitis

uncommon

51
Q

Signs, presentation, clinical evaluation in dogs with cholangitis/cholecystitis

A
  • Same as for cat with acute cholangitis
  • U/S to rule out obstruction
52
Q

dx for cholangitis/cholecystitis

A

Liver, bile (gallbladder mucosa) sampling
Histopathology
Culture

Cholecentesis (alternative)

53
Q

Obstruction at level of common bile duct

A
  • extrahepatic bile duct obtruction (EBDO)
    • Impedes bile flow into duodenum
  1. Complete obstructions (uncommon)
    • Acholic feces
    • Vitamin K responsive coagulopathy
    • Absence of urobilinogen in urine
  2. Incomplete obstructions (more common)
    • Clinicopathologic testing similar to other biliary disease
54
Q

underlying causes of exreahepatic bile duct obstruction

A
  • Extraluminal inflammatory conditions
    • ▪Most common cause in dogs
    • ▪Mild periductal edema, inflammation, scarring
  • Compressive lesions (relatively uncommon)
    • ▪Pancreatic neoplasia
    • ▪Biliary neoplasia
    • ▪Duodenal neoplasia
  • Diaphragmatic hernia
  • Cholelithiasis (rare)
55
Q

what could be causing gall bladder mucocele

A
  • Form of acute cholecystitis
  • May be associated with
    • Biliary obstruction
    • Gallbladder wall necrosis
    • Impending perforation
56
Q

characteristics of gallblader mucocele

A

Gallbladder distention and thickening
Sludge or intraluminal masses
STELLATE pattern to the sludge
Biliary obstruction can also be present

57
Q

signalment for gallblader mucocele

A

Smaller breeds and older dogs over represented

58
Q

cs for gallbladder mucocele

A
  • Nonspecific clinical signs
    • Vomiting, anorexia, lethargy
  • Most common physical exam findings
    • Abdominal pain, icterus, hyperthermia
59
Q

lab values for gallblader mucocele

A

Elevated bilirubin, ALT, ALP, GGT common
Biliary obstruction often present
Some only diagnosed at surgery
Gallbladder perforation common (50%)

60
Q

tx of choice for gallblader mucocele

A
  • Cholecystectomy –tx of choice
  • Medical treatment ??
    • Asymptomatic, normal bloodwork, incidental finding
    • Antibiotics and choleretics
    • Follow-up bloodwork, ultrasound examinations
61
Q

etiology for hepatic abscess

A
  • Septic embolization usually the cause
  • Most likely source -abdominal bacterial infection
  • Other sources possible (heart, lung, blood)
  • Predisposition –DM, hyperadrenocorticism
62
Q

clenical features for hepatic abscess

A

Older dogs
Anorexia, lethargy, vomiting
Fever, dehydration, abdominal pain
+/-hepatomegaly

63
Q

dx for hepatic abscess

A

Lab findings similar to other hepatobiliary disease
Ultrasound –imaging modality of choice
▪Anechoic, hypoechoic, hyperechoic, mixed
▪Usually have centralized anechoic to hypoechoic region
▪Poorly defined hyperechoic margin
▪FNA and cytology??

64
Q

tx and px for hepatic absces

A

Surgical removal of infected tissue (if focal)
Antibiotics (broad spectrum) –long term
Supportive care
Treatment of underlying condition
Prognosis
Guarded to fair

65
Q

nodular hyperplasia

define

dx

ddx

A

Benign condition of older dogs (no clinical signs)
Can be misinterpreted as more serious dz
May have elevated ALP (but normal bile acids)
Ultrasound
Variable appearance (up to 70% of older dogs)
Usually hypoechoic, but may be iso, hyper or mixed
Follow up ultrasound –monitor for changes
Liver cytology / biopsy
Serves to rule out neoplasia or other diseases
NOT to confirm hyperplasia

66
Q

common hepatic neoplasias

A

Primary neoplasia rare
Metastatic more common

Types
Hepatocellular carcinoma
Intrahepatic cholangiocellular carcinoma
Hepatocellular adenoma
Hemangiosarcoma
MCT
Lymphoma

67
Q

lab abnormalities as well as xx for hepatic neoplasia

A

Elevated liver enzymes –sometimes absent
Prognosis –Variable
Hepatocellular carcinoma
Complete resection –can have prolonged survival

68
Q

discuss hypertocutaneous syndrome

A

“Superficial necrolytic dermatitis”
“Metabolic dermatosis“
Uncommon disease -middle aged to older dogs
Skin lesions have characteristic histological changes
Superficial necrolytic dermatitis
Necrolytic migratory erythema
When combined with the hepatic changes, diagnosis of syndrome is made

69
Q

hepatic changes of of hepatocutaneous syndrome

A

Hepatic changes –honeycomb appearance to live

70
Q

discuss pathogenesis of hepatocutaneous syndrome

A

Pathogenesis of disease is still controversial
Affected dogs almost all have pronounced reductions in amino acid and albumin concentrations
Diabetes mellitus occurs in some dogs
Has also been associated with chronic long-term phenobarbital therapy
Most dogs presented because of skin disease
Abnormal liver enzymes, bile acids identified in most

71
Q

tx for hepatocutaneous syndrome

A

Intravenous amino acid solution (AminosynTM)
Dietary protein supplement (egg yolks, PROMOD)
Antibiotics (secondary skin infection)
Omega 3 fatty acids
Ursodiol
Vitamin E and/or zinc

72
Q

px for hepatocutaneous syndrome

A
  • Prognosis
  • Grave
  • Cause of death
    • ▪Liver dysfunction or severity of skin lesions, or both

sam dr green (10 decks)

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