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Important Features of Acquired and Congenital Hepatobiliary Disorders

Important Features of Acquired and Congenital Hepatobiliary Disorders

––––--ACQUIRED---------

––––-CONGENITAL---------

Early signs

Major bile duct occlusion

Severe hepatic insufficiency

PSVA, PSS

Microvascular dysplasiaa (no PSVA, microscopic shunting)

Ductal plate malformation

Vomiting

± Vomiting

± Vomiting

Abnormal behavior: lethargic

Liver ± small, low normal

Liver ± small, low normal size

Diarrhea/constipation

± Diarrhea/constipation

± Diarrhea/constipation

± Diarrhea/constipation

No clinicopathologic markers except ↑↑↑ bile acids

± Liver lobe hypoplasia

Weight loss

Weight loss

Weight loss

Weight loss

± Gallbladder atresia/hypoplasia

Pyrexia

Pyrexia

± Pyrexia

± Pyrexia

Protein C: normal (usually)

Predisposed to cholangitis

“Noisy enzymes”

Polydipsia

Polyuria/polydipsia

Polyuria/polydipsia

No hepatic encephalopathy

± Pyrexia if cholangitis

Normal bilirubinemia

Jaundice within 72 hours

Jaundice as disease advances

No jaundice

Variable liver enzymes:

most common ↑ ALT, ↑ALP

with inflammatory bowel disease

Variable enzymes:

↑ ALT, ↑ ALP

↑ with inflammatory bowel disease

Clear to yellow urine

↑ ALP & GGT

Variable ↑ ALP, AST, ALP, GGT

↓ RBC, MCV, ↓ BUN, ↓ creatinine

Normal bile acids

↑ ALT & AST, ↑ cholesterol

Gradual decline in cholesterol

↓ cholesterol

Variable liver enzymes

↓ cholesterol

No jaundice unless severe cholangitis

Polyuria/polydipsia

Orange urine

± neg urobilinogen: unreliable

Clear to orange urine

urobilinogen "+"

↑↑↑ bile acids

bruising/bleeding tendencies

Ammonium biurate crystalluria

Normal coagulation

↑↑↑ bile acids

No ammonium biurate crystalluria unless acquired portosystemic shunts form secondary to congenital hepatic fibrosis

Rarely dogs have PSVA—no ascites

Bleeding tendencies: 7–10 days

Brown to melenic feces

↓ Protein C (< 70%) often

Acholic (pale) feces

Brown feces

Copper-colored iris: cats

Melenic feces if GI bleeding

Green feces: ↑ stercobilin

Typically no ascites

Gastrointestinal ulceration

Normal to microhepatica: dog

Young dogs: melena—parasites

Hepatomegaly: firm; rounded borders

Hepatomegaly: cat

Microhepatica with “plump” kidneys

Palpable gallbladder: cat

if chronic: > 6 weeks

ascites

edema (rare in cats)

Gastroduodenal ulceration

associated with portal hypertension

ascites if: portal hypertension

ascites if: portal hypertension: ↓ albumin fosters ascites acquired portosystemic shunts

± Cryptorchid (small-breed dogs)

ptyalism (cats)

rare gastrointestinal ulceration: ↑ risk for hepatic encephalopathy

portal hypertension: only if intolerant to shunt ligation, true portal atresia, or arteriovenous malformation

ascites rare unless portal vein atresia or hepatic arteriovenous fistula

edema does not occur

HE: variable stupor, lethargy, depression

pacing, head pressing

rarely coma, seizures

hyperammonemia:

usually coincides with HE signs

ammonium biurate crystalluria

cystic/renal calculi

urinary tract obstruction

pollakiuria: urinary calculi

HE: common

tooth eruption bleeding →↑ risk HE

GI bleeding: parasites →↑ risk HE

amaurosis, stupor, depression, head pressing

pacing, aggression (esp cats), ptyalism

seizures with prolonged prodrome

hyperammonemia: usually coincides with HE

ammonium biurate crystalluria: common with HE

Ammonium urate cystic calculi: less common renal calculi may present for urinary obstruction →↑ BUN → NH3 →↑ risk HE

hematuria: due to urinary bladder calculi

aDoes not limit lifespan

PSVA, portosystemic vascular anomaly. PSS, portosystemic shunt. ALP, alkaline phosphatase. GGT, gamma glutamyl transferase. MCV, mean corpuscular volume. HE, hepatic encephalopathy.