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.

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.