Pathophysiology of Icterus and Hepatobiliary Disease Flashcards
1
Q
describe icterus
A
yellow skin, mucous membranes, and/or sclera due to bilirubin deposition
if you have icterus, by definition you have hyperbilirubinemia
also called jaundice, both terms acceptable
2
Q
describe hepatobiliary structure
A
- blood from portal vein and hepatic artery flows down sinusoids to the central vein
-portal vein drains the GI tract
-sinusoids lined by discontinuous endothelial cells - hepatocytes secrete bile, which flows into canaliculi and then to bile ducts
-central lobular hepatocytes have the most P450 enzymes to detox, so if tox, central guys affected first - gallbladder stores and concentrates bile
3
Q
describe the function of the liver
A
- produce and secrete bile
- bilirubin metabolism
- carbohydrate and lipid metabolism
- xenobiotic metabolism
- synthesize proteins and urea
- immune function
4
Q
describe the produce and secrete bile function of the liver
A
- bile function:
-excretion of waste
-facilitate digestion
-buffer acid ingesta - bile acids resorbed in ileum
- dysfunction:
-fat malabsorption (diarrhea)
-deficiency of fat-soluble vitamins
-acholic feces: clay colored due to lack of bile
5
Q
describe bilirubin metabolism
A
- primarily derived from hemoglobin
- bilirubin eliminated
-uptake
-conjugation
-secretion - dysfunction: hyperbilirubinemia/icterus
6
Q
describe causes of hyperbilirubinemia
A
- increased production/pre-hepatic
-hemolysis - failure of uptake/hepatic
-liver disease - failure to conjugate/hepatic
-liver disease, anorexia (horses>cattle) - defective secretion/post-hepatic:
-pancreatitis
7
Q
describe a gallbladder mucocele
A
- more common in dogs than cats
-increased incidence in shetland sheepdogs, mini schnauzers, cocker spaniels - risk factors:
-glucocorticoid treatment
-high fat diet - defective secretion of bile: post-hepatic hyperbilirubinemia
8
Q
describe the carbohydrate and lipid metabolism function of the liver
A
- removes glucose from blood
-stores as glycogen and fatty acids - production and degradation of plasma lipids
-cholesterol, triglycerides, phospholipids, lipoproteins - dysfunction:
-hypoglycemia
-hypocholesterolemia
9
Q
describe hepatic lipidosis
A
- numerous species susceptible
- excessive mobilization of fat in overconditioned animals due to a negative energy balance
- diagnosis does NOT equal metabolic syndrome
-can occur with some toxicities
-some lipid can be normal
10
Q
describe the xenobiotic metabolism function of the liver
A
1 cytochrome P450 enzyme functions
-convert to inactive metabolites
-bioactivate prodrugs into drugs
-generate reactive toxic metabolites
- species, breed, and sex differences
- excretion in bile or urine
- dysfunction:
-intoxication (wide range of diseases)
–hepatic necrosis
–photosensitization
–icterus
11
Q
describe pyrrolizidine alkaloid toxicosis
A
- in horses and cattle more than poultry and humans
- found in >6000 plant species
- cytochrome P450 metabolizes toxins into more reactive forms
- alkaloids bind to amino acids, proteins, nucleic acids
-inhibits DNA synthesis, mitosis - toxin activation leads to intoxication
for NAVLE:
-fibrosis
-megalocytosis
-biliary hyperplasia
12
Q
describe the synthesize proteins and urea function of the liver
A
- synthesizes a majority of plasma proteins
-albumin
-lipoproteins
-clotting factors (II, V, VII-XIII) - converts ammonia to urea
- dysfunction:
-hypoalbuminemia, effusion
-coagulopathy
-hepatic encephalopathy
-PU/PD
13
Q
describe hepatic encephalopathy
A
- due to portosystemic shunts, liver failure (plant toxicities, chronic disease)
-overproduction of ammonia from the gut can occur in horses - ammonia metabolized by astrocytes, resulting in free radical production and cytotoxic brain edema
- inability to metabolize ammonia and likely other neurotoxins
14
Q
describe clinical hepatobiliary disease
A
3 broad categories
- hepatocellular damage
- cholestais
- hepatic insufficiency
15
Q
describe hepatocellular damage
A
- damaged focused on hepatocytes
- diverse causes of damage
-inflammation: pathogens, secondary to necrosis
-degeneration: hypoxia, congestion
-necrosis: pathogens, toxins
-neoplasia
16
Q
describe histomonas meleagridis
A
- turkeys, chickens, peasants, peafowl
- numerous routes of transmission
-ingestion of heterakis gallinarium (HG)
-ingestion of earthworms infected with HG
-direct contact via cloaca - HG localize cecum and molt, releasing H. meleagridis trophozoites
- trophozoites invade cecal wall, followed by vascular dissemination to the liver
- hepatocellular necrosis/damage
17
Q
describe cholestasis
A
- damage focused on bile ducts and hepatocytes adjacent to affected bile ducts/canaliculi
- cholestasis = disturbance of bile flow
-can occur within and outside the liver - associated with hyperbilirubinemia
18
Q
describe liver flukes
A
- fasciola hepatica: cattle, sheep
-fascioloides magna: white tailed deer and elk - snail = intermediate host
- host ingests larvae and migrate to liver to mature in bile ducts
- inflammation and obstruction of bile ducts = cholestasis
- clostridium novyi, C. hemolyticum spores proliferate in damaged liver, resulting in hepatocellular damage
19
Q
describe hepatic insufficiency
A
- loss of productive capacity
- portosystemic shunts, liver failure
-acute: pathogens, drugs, toxins
-chronic: idiopathic, drugs, toxins - can be consequence of hepatocellular damage
20
Q
describe congenital portosystemic shunt
A
- intrahepatic or extrahepatic
- common in dogs
-infrequent in cats, horses, cattle - diminished blood supply to liver leads to impaired ability to function
21
Q
describe cirrhosis
A
- better called end-stage liver disease; due to chronic toxicity, cholangitis and/or obstruction, congestion, disorder of metal metabolism, hepatitis, and/or idiopathic
- can be associated with acquired PSS
- inadequate number of functional hepatocytes leads to impaired ability to function
22
Q
describe species differences in livers
A
- cows: 3 lobes only
- alpacas: weird nodular things = completely nornal
23
Q
describe hepatobiliary eval
A
- float in formalin = lipidosis
- gallbladder patent?
-distended but patent: fasting
-distended but not patent: obstruction - cut surface:
-like with intestines
