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63 Cards in this Set

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What are the components of the normal portal tract?
hepatic a., portal v. , bile duct, lymphatics, nerves, CT (collagen type I)

limiting plate: border of hepatocytes that form outer boundary of portal tract
What makes up the lobule model of the liver?
hexagon bordered by 6 portal tracts w/ central vein in middle

3 areas: periportal, midzonal, centrilobular
What are Kupffer cells?
hepatic MPs that sit on endo cells of sinusoids & filter blood borne material
What are stellate cells?
= lipocytes, Ito cells

sinusoidal lining cells that store vitamin A, can synthesis collagen when activated
What are 3 portal of entry to the liver resulting in injury?
direct extension: penetrating trauma thru abd. wall or thru GI tract (ex. cattle w/ TRP)

hematogenous: localization w/in sinusoids, Kupffer cells, or capillary bed of GB

retrograde biliary transport: ascending bacterial or parasitic infections
Describe a random pattern of hepatocellular degeneration & necrosis.
single cell necrosis or MF aggregates of necrotic cells

typical of blood-borne infectious agents

inflammation: viral (little), bacterial (suppurative), Mycobacteria (granulomatous)
Describe a centrilobular pattern of hepatocellular degeneration & necrosis.
around central v. (most common type)

hypoxic injury occurs here 1st

most toxic drugs produce injury here
What are 3 main causes of hyperbilirubinemia?
1. overproduction thru hemolysis (hemolytic anemia, intestinal hemorrhage)
2. ↓ uptake by hepatocytes (hepatocellular dz, fasting horses)
3. ↓ outflow of bile (cholestasis: obstruction, hepatocellular dz)
What are the 2 main patterns of cholestasis & what are the causes of each?
1. extrahepatic
-intralumenal obstruction: choleliths, parasites, stricture, inspissated bile, GB mucocele
-extralumenal obstruction: neoplasm, abscess
-histology
*acute: distension of bile ducts, edema, mild portal inflammation
*chronic: circumferential bile duct fibrosis to biliary cirrhosis

2. intrahepatic: assoc. w/ hepatocyte disorders affecting ability to metabolize & excrete bile
-histology: canalicular stasis (bile plugs)
What is the pathogenesis of liver fibrosis?
hepatic injury --> stellate cells take on a myofibroblast form --> lose vitamin A storing function --> begin synthesis of collagen I

can lead to portal hypertension
What is the significance of biliary hyperplasia?
common nonspecific response to liver injury
What is the pathogenesis of end-stage liver or cirrhosis?
significant liver injury --> architecture of lobules lost & replaced by regenerative nodules surrounded by bands of fibrosis & often bile duct hyperplasia --> liver failure, portal hypertension, ascites
What are some causes of end-stage liver or cirrhosis?
chronic toxicity, chronic cholangitis &/or obstruction, chronic congestion (R heart failure), inherited disorders of metal metabolism (Cu, Fe), chronic hepatitis, idiopathic
What metabolic distubrances are associated w/ liver injury?
hypoglycemia
acidosis
sepsis
coag disorders
hypoalbuminemia
What is hepatocutaneous syndrome?
-crusting, erosions, ulceration of muzzle, face, footpads, & pressure points in some dogs w/ severe hepatic dz
-characteristic multinodular livers, often w/ little fibrosis b’twn nodules
-cause: unknown

= superficial necrolytic dermatitis
What is the regeneration capacity of the liver?
liver has extraordinary ability to regenerate

if injury is severe enough or repeated such that ECM is destroyed --> regeneration cannot reform into normal liver --> nodules replace missing mass (have abnormal blood supply, drainage, & disrupted biliary flow --> altered liver function)
What is primary photosensitiziation?
from eating plants w/ preformed photodynamic agents (ex. St. John’s Wort), or some drugs (NOT a result of hepatic dz)
What is secondary photosensitization?
hepatogenous: occurs in herbivores

-phylloerythrin: naturally occurring photodynamic pigment in plants that is normally cleared from portal blood by liver

-liver dz --> accumulation of phylloerythrin in blood & tissues --> tissue injury when exposed to UV light
What is the main function of the exocrine pancreas & what is the most common sign of dysfunction?
secretions conducted to duodenum via pancreatic ducts --> aid in digestion of protein, fat, carbs

maldigestion = dysfunction
What are some development anomalies associated w/ the liver?
congenital biliary cysts: common in cats (ddx: parasitic cysts, biliary adenomas); usually NGS

hepatic displacement: diaphragmatic hernias (congenital or traumatic)
What are the consequences of inadequate hepatic blood flow?
atrophy, telangiectasis, infarction
What is the cause of passive congestion of the liver & what are the acute & chronic pathologic manifestions?
R heart failure --> backup of blood in caudal vena cava & hepatic congestion

acute: congestion in centrilobular areas, atrophy of centrilobular hepatocytes, liver enlarged

chronic: centrilobular fibrosis, “nutmeg liver” (common in old dogs w/ endocardiosis)
What is hepatic veno-occlusive dz?
partial to complete occlusion of central vv. --> portal hypertension
What are the 2 types of portosystemic shunts?
1. extrahepatic: shunt occurs before portal v. enters liver
-usually a single vessel connecting portal v. w/ caudal vena cava, renal v., or azygous v.
-most commonly found in small breed dogs; also cats, other species

2. intrahepatic: usually result of a patent ductus venosus
-most commonly found in large breed dogs
What are the hepatic, pre-hepatic, & post-hepatic causes of portal hypertension?
hepatic: fibrosis along sinusoids --> collapse or stenosis, portal v. hypoplasia (young dogs & cats affected), intrahepatic arterior-venous fistula

pre-hepatic: thrombosis, tumor mets, parasites, abscesses --> restricted flow thru portal v.

post-hepatic: CHF --> inc. resistance to outflow of blood thru hepatic v.
What are the consequences of portal hypertension?
usually numerous shunt vessels, ascites (d/t ↑ pressure w/in portal v. & liver)

associated parenchymal disorders: hepatic fibrosis, cirrhosis (lobular dissecting hepatitis)
lobular dissecting hepatitis

a. signalment
b. clinical signs
c. gross lesions
d. histo lesions
a. young dogs
b. ascites, hypoalbuminemia, ↑ liver enzymes, ↑ bile acids (rapidly fatal)
c. small smooth livers, multiple portosystemic collaterals, portal hypertension
d. micronodules, diffuse disruption of hepatic architecture, diffuse infiltration of inflammatory cells
What are 3 causes of hepatic lipidosis assoc. w/ increased inflow?
1. excess dietary fat --> excess entry of FAs into liver
2. ↑ mobilization of TGs from adipose tissue d/t ↑ demand (lactation, starvation, endocrine abnormalities)
3. excess dietary carbs --> ↑ FA synthesis --> excessive TGs w/in hepatocytes
What are 2 causes of hepatic lipidosis assoc. w/ abnormal metabolism?
abnormal hepatocyte function (mitochondrial injury) --> ↓ energy for oxidation of FAs w/in hepatocytes --> accumulation of TGs w/in hepatocytes

↑ glucose & insulin levels --> ↑ esterification of FAs to TGs
What are 2 causes of hepatic lipidosis assoc. w/ decreased excretion?
↓ apoprotein synthesis --> ↓ production & export of lipoprotein from hepatocytes

hepatotoxins or drugs --> secretory defects --> impaired secretion of lipoprotein from liver
What are the 3 broad categories of causes of hepatic lipidosis?
increased inflow of fat

abnormal metabolism of fat

decreased excretion of fat
What is steroid hepatopathy?
glucocorticoid induced hepatocellular degeneration

excessive amts of endogenous or exogenous glucocorticoids --> marked swelling of hepatocytes d/t accumulation of glycogen

grossly, liver is yellowish, pale & enlarged (ddx: fatty liver)
What is a cause of hepatic copper accumulation in dogs?
hereditary disorders of copper metabolism occur in Bedlington terriers, Westies, Skye terriers, Dobermans, etc. --> chronic copper accumulation & liver dz --> chronic hepatitis & fibrosis
What pigments may accumulate in the liver?
bile: from cholestasis
hemosiderin: hemochromatosis: hepatic injury d/t excess iron accumulation
lipofuscin: residue of incompletely digested lipids (cell mems)
melanin: esp. in lower vertebrates, congenital in swine, sheep
fluke pigment: Fasciola most common
infectious canine hepatitis

a. etiologic agent
b. histological lesions
c. gross lesions
a. canine adenovirus I
b. centrilobular necrosis: unusual for viral infection, characteristic basophilic intranuclear inclusions in hepatocytes & endothelial cells
c. petechiae & ecchymoses on serosal surfaces d/t vascular necrosis, +/- blue eye
herpes virus

a. associated hepatic lesions
b. etiologic agents
a.MF random hepatic necrosis w/o inflammation, petechiae, ecchymoses

b. equine herpes virus 1, bovine rhinotracheitis, canine herpes, feline rhinotracheitis (neonates usually affected)
What are 2 hepatic lesions associated w/ nematodes?
larval migration thru liver is common --> focal fibrosis (“milk spotted liver”): ascarids, strongyles, Stephanurus dentatus

vena caval syndrome: Dirofilaria immitis adults collect in caudal vena cava --> severe intravascular hemolysis, DIC, acute hepatic failure
What is the most common type of cholangitis & what is the most common cause?
neutrophilic cholangitis: neutrophils in lumen or w/in epi cells of bile ducts

usually caused by ascending bacterial infection from GI tract
lymphocytic cholangitis

a. species affected
b. histological lesions
a. chronic idiopathic cholangitis of cats
b. moderate to dense lymphocytic & plasmacytic infiltrates of portal areas
+/- biliary proliferation & portal fibrosis
What is the pattern of injury seen w/ toxic liver injury & why?
centrilobular b/c enzymes involved in bioactivation are in highest concentrations there
What are some causes of acute liver toxicity?
blue green algae (preformed toxins)
plants
mycotoxins (aflatoxin B: Aspergillus flavus: acute in dogs, chronic in LA)
toxic mushrooms: Amanita spp
chemicals: phosphorous, carbon tetrachloride, cresols, metals
therapeutic drugs: acetaminophen, diazepam in cats; Trimethoprim-sulfa ABs, Carprofen
Why are cats particularly susceptible to acetominophen toxicity?
weak phase 2 enzyme activity (relatively deficient in glucuronyltransferase activity: forms conjugates b’twn bioactivated xenobiotics & glutathione)
What are some causes of chronic hepatic toxicity?
plants: pyrrolizidine alkaloids
therapeutic drugs: anticonvulsants in dogs
Pyrrolizidine alkaloids

a. how they cause hepatic injury
b. characteristic lesion
a. must be metabolized into alkylating agents to cause toxic injury

b. megalocytes: enlarged hepatocytes w/ very large dark staining nuclei
hepatocellular nodular hyperplasia

a. cause
b. gross appearance
a. normal, age related in dogs (starts at ~6 yrs)
b. solitary to multiple pale yellow to red-brown nodules in otherwise healthy liver, well circumscribed
What are regenerative hepatic nodules?
proliferative nodules in diseased, usually fibrotic livers

usually only a single portal tract w/in each nodule
Describe the prevalence & gross appereance of:

a. hepatocellular adenoma
b. hepatocellular carcinoma
a. uncommon benign, usually solitary mass (gross ddx in dog: nodular hyperplasia)
b. uncommon, friable, gray to yellow masses divided into lobules (mets uncommon)
cholangiocellular adenoma

a. species most commonly affected
b. cystic variants
a. cat
b. produce very large masses composed of fluid filled cysts
cholangiocellular carcinoma

a. gross appearance
b. histologic appearance
c. biological behavior
a. firm, umbilicated large single mass or multiple masses
b. ducts or acini lined by poorly differentiated cuboidal biliary epithelium
c. mets very common: aggressive tumor
What are carcinoids?
tumors in dogs & cats derived from neuroendocrine cells in biliary tree; highly metastatic
ddx for nodular liver
nodular hyperplasia
regenerative nodules
hepatocellular adenoma
hepatocellular carcinoma
biliary carcinoma
metastasis
What are some causes of biliary obstruction?
choleliths
parasites
stenosis d/t local tumors or abscesses
cholecystitis

a. etiologies
b. acute
b. chronic
a. canine adenovirus I, Rift Valley fever, Salmonella
b. characteristic edema & hemorrhage
c. usually accompanies prolonged bacterial infection or ongoing irritation by choleliths or parasites
-rarely GB can rupture --> severe peritonitis
What is a gallbladder mucocele?
distended gall bladder filled w/ a mucus plug (cause unkown)
What is cystic mucinous hyperplasia of the gall bladder?
hyperplastic lesion of gall bladder epi in old dogs (no clinical significance)
pancreatic hypoplasia (juvenile pancreatic atrophy)

a. signalment
b. clinincal signs
c. lesion
a. occurs in several dog breeds, esp. GSD & sporadically in calves
b. signs of EPI appear at 6-12 mos: thin despite voracious appetite, persistent diarrhea
c. exocrine pancreas dramatically diminished in size --> inadequate function
What are Pacinian corpuscles?
small pale nodules (clear spots) in cat pancreas that are pressure sensors (normal)
What are some causes of pancreatic degeneration?
prolonged anorexia or starvation
obstruction of pancreatic ducts (calculi, parasites, local neoplasms or abscesses)
chronic pancreatitis --> loss of zymogen granules
What are some causes of acute pancreatitis/pancreatic necrosis?
obstruction of pancreatic ducts by parasite migration or calculi
delivery of blood-borne toxins (uremic toxins) or therapeutic drugs (ex. Sulfonamides)
ischemia from a variety of causes --> direct injury to acinar cells
direct trauma to pancreas
aberrant transport of proenzymes w/in acinar cells --> inappropriate activation of enzymes w/in cells
consumption of high fat meal
hypercalcemic conditions (ex. hyperparathyroidism)
What are some possible sequelae to acute pancreatitis?
release of inflammatory mediators can cause widespread vascular injury, hemorrhage, DIC, shock, ARDS
chronic pancreatitis

a. most common cause in dogs
b. lesions
c. possible sequelae
a. series of mild episodes of acute pancreatitis
b. fibrosis & parenchymal atrophy, fibrous adhesions to adjacent organs, saponification of mesenteric fat
c. EPI, DM (horses) can occur if severe
What is pancreatic nodular hyperplasia?
age related change in old cats, dogs, cattle (no clinical significance)

raised smooth gray-white masses
pancreatic carcinoma

a. species most commonly affected
b. gross appearance
b. biologic behavior
a. dogs & cats
b. gray to yellow, invasive masses w/ abundant adhesions
c. mets common: aggressive tumor