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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
discuss efficacy of anti-fibrotic medications in chr. hepatitis
**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
26
discuss goals of dietary modification in chr. hepatits therapy
* 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
27
list the hepatoprotectants that may be used in chr. hepatitis
* vit e * hepatoproctactant, antioxidative * S-adenosyl methionine (SAMe, Denosyl) * Hepatoprotectant, glutathione source * Ursodiol (Actigall) * has antiinflamatory effects * Milk thistle?
28
px for chronic hepatitis
* 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)
29
Poor prognostic indicators for chronic hepatits
* Hypoalbuminemia, hypoglycemia, coagulopathies * Cirrhosis (survival \< 1 month in one study)
30
how do dogs present with congenital portosystemic shunts
* Presentation similar to cats * may be presenting with neurological signs, * urinary signs smaller than other litter mates
31
signalment for portosystemic shunts in dogs
* Small breed dogs most commonly affected * Yorkshire Terrier
32
what type of portosystemic shunt occurs in large breed dogs
intrahepatic shunt
33
what type of portosystemic shunt occurs in small breed dogs
Single extrahepatic shunts
34
what kind of shunt do cats get
single extra hepatic shunt
35
dx,tx and px for portosystemic shunts in dogs possible complications
* 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
definition for microvascular dysplasia
* Clinical features of PSS with no vascular anomaly * Normal imaging (u/s,portogram, scintigraphy) * Microscopic vascular anomaly
37
signalment for microvascular dysplasia
Same breeds affected with PSS
38
tx for microvascular dysplasia
No surgical treatment Treat only if and when signs of hepatic encephalopathy occur
39
how common are primary biliary dz in dogs
* Rare in dog * More common in cat
40
causes of secondary biliary dz in dogs
* Pancreatitis (common cause) * Sepsis (from non hepatobiliary disease)
41
More common biliary tract disorders
* Extrahepatic bile duct obstruction (EBDO) * Bile peritonitis * Gallbladder mucocele * **All require surgical intervention**
42
clinical features of biliary tract disorders
* Icterus * Acute / chronic vomiting * Anorexia, depression, weight loss * +/-abdominal pain
43
dx for biliary tract disorders
* Bloodwork –increases in * ▪Bilirubin * ▪ALP, GGT * ▪ALT (less severe) * Cholestatic process
44
what can u see on rads with biliary disorders
* Pancreatitis * Loss of serosal detain in cranial abdomen * Lateral displacement of duodenum * Cholelithiasis * Limitations?
45
when is US useful in biliary dz dx
Differentiate hepatic vs. post hepatic icterus Is it a surgical case? **Yellow animal with no anemia –ULTRASOUND**!
46
can u use Serial bilirubin levels to determine if surgical case?
no
47
tx for non obstructive biliary dz
* Supportive care * Antibiotics, vitamin K PRN
48
tx for obstructive biliary disorders
Surgery (biliary reconstruction PRN) Biopsy Culture
49
Inflammation of bile ducts
uncommon cholangitis
50
Inflammation of gallbladder
Cholecystitis uncommon
51
Signs, presentation, clinical evaluation in dogs with cholangitis/cholecystitis
* Same as for cat with acute cholangitis * U/S to rule out obstruction
52
dx for cholangitis/cholecystitis
Liver, bile (gallbladder mucosa) sampling Histopathology Culture Cholecentesis (alternative)
53
Obstruction at level of common bile duct
* **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
underlying causes of exreahepatic bile duct obstruction
* 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
what could be causing gall bladder mucocele
* Form of **acute cholecystitis** * May be associated with * Biliary obstruction * Gallbladder wall necrosis * Impending perforation
56
characteristics of gallblader mucocele
Gallbladder distention and thickening Sludge or intraluminal masses STELLATE pattern to the sludge Biliary obstruction can also be present
57
signalment for gallblader mucocele
Smaller breeds and older dogs over represented
58
cs for gallbladder mucocele
* Nonspecific clinical signs * Vomiting, anorexia, lethargy * Most common physical exam findings * Abdominal pain, icterus, hyperthermia
59
lab values for gallblader mucocele
Elevated bilirubin, ALT, ALP, GGT common Biliary obstruction often present Some only diagnosed at surgery Gallbladder perforation common (50%)
60
tx of choice for gallblader mucocele
* Cholecystectomy –tx of choice * Medical treatment ?? * Asymptomatic, normal bloodwork, incidental finding * Antibiotics and choleretics * Follow-up bloodwork, ultrasound examinations
61
etiology for hepatic abscess
* Septic embolization usually the cause * Most likely source -abdominal bacterial infection * Other sources possible (heart, lung, blood) * Predisposition –DM, hyperadrenocorticism
62
clenical features for hepatic abscess
Older dogs Anorexia, lethargy, vomiting Fever, dehydration, abdominal pain +/-hepatomegaly
63
dx for hepatic abscess
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
tx and px for hepatic absces
Surgical removal of infected tissue (if focal) Antibiotics (broad spectrum) –long term Supportive care Treatment of underlying condition Prognosis Guarded to fair
65
nodular hyperplasia define dx ddx
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
common hepatic neoplasias
Primary neoplasia rare Metastatic more common Types Hepatocellular carcinoma Intrahepatic cholangiocellular carcinoma Hepatocellular adenoma Hemangiosarcoma MCT Lymphoma
67
lab abnormalities as well as xx for hepatic neoplasia
Elevated liver enzymes –sometimes absent Prognosis –Variable Hepatocellular carcinoma Complete resection –can have prolonged survival
68
discuss hypertocutaneous syndrome
“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
hepatic changes of of hepatocutaneous syndrome
Hepatic changes –honeycomb appearance to live
70
discuss pathogenesis of hepatocutaneous syndrome
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
tx for hepatocutaneous syndrome
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
px for hepatocutaneous syndrome
* Prognosis * Grave * Cause of death * ▪Liver dysfunction or severity of skin lesions, or both

sam dr green (10 decks)

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