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Module 16 > Patterns of Hepatobiliary & Pancreatic Disease in Dogs & Cats > Flashcards

Patterns of Hepatobiliary & Pancreatic Disease in Dogs & Cats Flashcards

1
Q

what are the 7 critical functions of the liver

A
  1. bilirubin metabolism
  2. bile acid metabolism
  3. carbohydrate metabolism
  4. lipid metabolism
  5. xenobiotic metabolism (bioactivation, detoxification)
  6. protein synthesis (albumin, globulins, apoproteins, clotting factors)
  7. immune function
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2
Q

describe the architecture of the liver

A
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3
Q

what is the zonal organization of the hepatic lobule

A

periportal area (zone 1)

midzonal area (zone 2)

centrilobular area (zone 3)

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4
Q

describe how the zonal organization of the hepatic lobulue

A
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5
Q

what is shown here

A

PV = portal vein

LP = limiting plate

BD = bile duct

HA = hepatic artery

LV = lymphatic vessel

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6
Q

what are the functions of fenestrated endothelial cells

A

dynamic filter of plasma proteins, solutes and particulate matter

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7
Q

what is the function of kupffer cells

A

phagocytosis

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8
Q

what are the functions of stellate cells

A

lipid and vitamin storage, fibrosis (reparative response to injury through myofibroblast transformation and fibrosis)

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9
Q

how is bilirubin metabolized (10)

A
  1. senescent erythrocytes
  2. phagocytozed by macrophages in splee, bone marrow, and liver
  3. globin portion degraded within macrophages (constituents returned to the amino acid pool)
  4. heme Fe transferred to Fe-binding proteins such as trasnferrin for recycling
  5. remaining portion of heme
  6. biliverdin
  7. bilirubin (circulating bound to albumin)
  8. uptake by hepatocytes
  9. glucuronydation
  10. bile excretion
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10
Q

what are the ezymes that are secreted as inactive proenzymes (6)

A
  1. trypsin
  2. chymotrypsin
  3. collagenase
  4. phospholipase
  5. elastases
  6. carboxypeptidases
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11
Q

what are the enzymes that are secreted as active enzymes

A

amylase

lipase

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12
Q

what are the liver vascular anomalies in the dog (3)

A
  1. portosystemic shunts (PSSs)
  2. congenital extrahepatic shunts
  3. intrahepatic shunts
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13
Q

what is a congenital extrahepatic shunts

A

shunting from portal vein or major tributaries (left gastric or splenic veins, less commonly gastroduodenal or mesenteric veins) to the caudal vena cava (portocaval shunt) or to the azygous vein (portoazygous shunt)

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14
Q

what are intrahepatic shunts

A

located in left hepatic division

persistent patent fetal ductus venosus

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15
Q

what type of hepatic shunts are common in large breed dogs

A

typically large intrahepatic shunts

usually patent ductus venosus, but sometimes large intrahepatic communications

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16
Q

what hepatic shunts are common in small breed dogs

A

single large extrahepatic shunts between portal vein and vena cava or azygous vein

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17
Q

how do acquired portosystemic shunts occur (4)

A
  1. chronic liver disease
  2. periportal fibrosis
  3. portal hypertension
  4. development of multiple tortuous shunting vessels
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18
Q

what is shown here

A

acquired portosystemic shunt

multiple tortuous shunting vessels

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19
Q

what is primary portal vein hypoplasia

A

affected extrahepatic or intrahepatic portal vein (or both) accompanied by portal hypertension with a development of multiple collateral portosystemic shunts

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20
Q

what is congenital hepatoportal microvascular dysplasia

A

without accompanying macroscopic portosystemic shunts

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21
Q

what breeds is congenital hepatoportal microvascular dysplasia seen in

A
  1. cairn terriers
  2. yorkies
  3. maltese
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22
Q

what are histological features of portosystemic shunts (5)

A
  1. hepatocellular atrophy
  2. closely and unevenly spaced portal triads

3. portal triads with attenuated or absent portal vein profiles

4. proliferation/reduplication or portal arterioles

  1. possible bile duct proliferation
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23
Q

what histological change is seen here

A

proliferation of portal arterioles

absence of portal vein

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24
Q

what are the clinical presentation of congenital shunts (3)

A
  1. failure to thrive
  2. neurological signs (hepatic encephalopathy)
  3. history of depression, convulsions, and other nervous signs exacerbated by a high protein diet, and may be alleviated by dietary control
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25
Q

what are the presenting signs of acquired shunts

A

with chronic liver disease resulting in portal hypertension

  1. elevation of liver enzymes serum levels
  2. possible ascites
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26
Q

what are the toxins implicated in hepatic encephalopathy (11)

A
  1. ammonia
  2. aromatic amino acids
  3. bile acids
  4. decreased alpha ketoglutaramate
  5. endogenous benzodiazepines
  6. false neurotransmitters
  7. GABA
  8. glutamine
  9. phenol
  10. short chain fatty acids
  11. tryptophan
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27
Q

what type of virus is canine adenovrius 1

A

DNA virus

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28
Q

what tropism does canine adenovirus have

A

for endothelium, mesothelium and hepatocytes

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29
Q

what is the clinical presentation of canine adenovirus 1 (5)

A
  1. fever
  2. vomiting and melena (in severe cases)
  3. abdominal pain
  4. corneal opacity (edema) in chronic cases (possible spontaneous resolution)
  5. rare peracute cases –> sudden death without clinical manifestations
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30
Q

what are some gross pathological changes to the liver caused by canine adenovirus 1 (4)

A
  1. granular appearance of serosal surface
  2. scattered petechial or blotchy serosal hemorrhages
  3. liver enlarged (but with sharp edges) and friable
  4. fibrin strands on liver surface, particularly between lobules
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31
Q

what other gross pathological changes can be seen in the rest of the GI tract following canine adenovirus 1 (3)

A
  1. small amounts of blood tinged fluid the abdomen
  2. gallbladder wall thickening (edema)
  3. hemorrhages in other organs (kindey, lung) variable
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32
Q

what is the likely cause of these pathological changes

A

dog CAV-1 infection

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33
Q

what is changes are seen here and what is the likely cause

A

fibrin tags on liver lobes

gall bladder wall thickened by edema

CAV-1 infection

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34
Q

what histopathological changes are seen here and what is the likely cause

A

hepatocellular necrosis and loss

intranuclear viral inclusion bodies

dog CAV-1 infection

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35
Q

what can cause chronic hepatitis in dogs (3)

A
  1. viruses
  2. bacteria
  3. toxins
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36
Q

what is copper associated with in dogs

A

implicated in progressive necro-inflammatory canine liver disease with breed related susceptibility

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37
Q

what are inflammatory infiltrates dominated by in chronic hepatitis in dogs (2)

A
  1. CD3+
  2. T-cells
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38
Q

what damages does chronic hepatitis in dogs cause to the liver (2)

A
  1. hepatocellular necrosis and loss
  2. progression to parenchymal collapse and fibrosis
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39
Q

what mechanisms might contribute to chronic hepatitis in dogs

A

immune mediated/autoimmune mechanisms

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40
Q

what type of inflammation does a primary hepatopathy cause (5)

A

moderate to marked inflammatory inflitrate of

  1. lymphocytes
  2. plasmacytic
  3. neutrophilic
  4. granulomatous
  5. eosinophilic
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41
Q

what type of damage does a primary hepatopathy cause

A

necrosis/apoptosis

+/- ductular proliferation

+/- fibrosis

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42
Q

what is the clinical scenario with primary hepatopathies (2)

A
  1. moderate to severe increased ALT
  2. +/- abnormal function tests
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43
Q

what type of infiltrate does chronic hepatitis cause (4)

A

mild to moderate inflammatory infiltrate

  1. lymphcytic
  2. neutrophilic
  3. granulomatous
  4. eosinophilic
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44
Q

what damage is seen in chronic hepatitis (3)

A
  1. necrosis/apoptosis
  2. portal-portal or portal-central fibrosis with lobular architechture distortion
  3. regenerative nodules (micronodular or macronodular)
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45
Q

whta is the clinical scenario with chronic hepatitis (6)

A
  1. increased total serum bile acids
  2. hyperbilirubinemia
  3. hypoalbuminemia
  4. +/- ascites
  5. acquired portosystemic shunts
  6. portal hypertension
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46
Q

what type of inflammation does a secondary hepatopathy cause (4)

A

mild to moderate portal inflammation

  1. lymphocytic
  2. plasmocytic
  3. neutrophilic
  4. granulomatous
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47
Q

is there necrosis/apoptosis with a secondary hepatopathy

A

no

48
Q

is there fibrosis with a secondary hepatopathy

A

no

49
Q

is there architechtural remodelling with a secondary hepatopathy

A

no

50
Q

what is the clinical scenario of a secondary hepatopathy

A
  1. ALT/ALP 3x upper limit of normal
  2. normal function tests
51
Q
A
52
Q

what are the most common causes of canine chronic hepatitis

A
  1. immune
  2. toxic –> copper
  3. infectious is uncommon
53
Q

what are the most common clinical signs of chronic hepatitis (13)

A
  1. decreased appetite
  2. lethargy/depression
  3. icterus
  4. ascites
  5. PU/PD
  6. vomiting
  7. diarrhea
  8. hepatic encephalopathy
  9. melena
  10. abdominal pain
  11. gingival bleeding
  12. hematochezia
  13. hemoperitoneum
54
Q

what are the clinical pathologies that are most commonly seen in chronic hepatitis (8)

A
  1. increase ALT
  2. increased ALP
  3. increased ASP
  4. increased GGT
  5. increased total serum bile acids
  6. decreased BUN
  7. decreased albumin
  8. decreased cholesterol
55
Q

what is consistently seen in hematology and clinical chemistry in chronic hepatitis

A

increased ALT and ALP

in most cases increased in AST, GGT, bilirubin and resting BAs

decreased albumin and urea

increased PT and PTT

56
Q

what histological changes are seen in chronic hepatitis (5)

A
  1. portal and parenchyma inflammation (mainly lymphocytes and plasmacells)
  2. hepatocyte necrosis/apoptosis associated with inflammation
  3. variable periportal to bridging fibrosis
  4. copper accumulation in the periportal regions (secondary to cholestasis)
  5. no infectious agents (viruses or bacteria) identified
57
Q

what is DLA

A

dog leukocyte antigen

central role in control of the immune system

regulation/presentation of self and non self antigens to the immune system

58
Q

what is DLA involved in with chronic hepatitis

A

associated with susceptibility/resistence to chronic hepatitis in english springer spaniels

increased risk of chronic hepatitis

59
Q

what is copper essential for

A

cofactor for enzymes and cellular functions

60
Q

what is copper homeostasis regulated by (4)

A
  1. uptake in the GI tract
  2. intra and extra cellular trafficking system
  3. distribution through the body (bound to ceruloplasmin)
  4. cellular storage (metallothionein) and excretion (mainly in the bile)
61
Q

what breed has genetic basis for copper associated canine liver disease

A

bedlington terriers

autosomal recessive gene deletion which has an important role in copper biliary excretion

62
Q

what other breeds have a predisposition of copper associated liver disease (5)

A
  1. dobermann
  2. west highland white terrier
  3. skye terrier
  4. dalmation
  5. lab retriever
63
Q

how is copper associated liver disease diagnosed

A
  1. determination of copper levels in fresh liver tissue sample
  2. histopathology, special strains (Rhodanin/rubeanic acid)
64
Q

where is primary copper accumulation in the liver

A

centrilobular

65
Q

where is the secondary to chronic liver injury copper accumulation

A

secondary is mainly periportal

66
Q

what are the clinical signs of copper associated chronic hepatitis (10)

A
  1. exercise intolerance
  2. depression
  3. anorexia
  4. vomiting
  5. weight loss
  6. polyuria/polydipsia
  7. icterus
  8. diarrhea
  9. ascites
  10. salivation
67
Q

what are the clinical findings with copper assocaited with chronic hepatitis in dogs (2)

A
  1. hemolysis from Cu release into blood (only bedlington terriers)
  2. serum biochemistry abnormaities (increase in ALT higher than ALP)
68
Q

what are toxic causes of liver disease in dogs (3)

A
  1. xylitol
  2. amanitin
  3. microcystin-LR (from blue green algae)
69
Q

what are therapeutic drugs that can cause liver disease in dogs (4)

A
  1. trimethoprim-sulfonamide
  2. mebendazole (antiparasitic)
  3. anticonvulsant drugs (primidone, phenytoin, phenobarbital)
  4. carprofen
70
Q

what causes endogenous steroid induced hepatopathy

A

cushing’s syndrome

71
Q

how does cushing’s disease lead to steroid induced hepatopathy

A

hyperadrenocorticism (possibly related to ACTH secreting pituitary tumour) –> sustained increased levels of circulating glucocorticoids

intracytoplasmic accumulation of glycogen and fluid –> marked hepatocellular swelling/vacuolation

72
Q

what is shown here in the liver

A

marked hepatocellular swelling/vacuolation from endogenous steroid induced hepatopathy

73
Q

what are the types of steroid induced hepatopathy

A
  1. iatrogenic: prolonged admin of corticosteroids
  2. endogenous: cushing’s
74
Q

what is suppurative cholangitis/cholangiohepatitis common in

A

mature/aged cats 11-15 years

less common in dogs

75
Q

what is the acute phase of suppurative cholangitis/cholangiohepatitis (2)

A
  1. inflammation and degeneration of bile ducts
  2. inflammation extending into lobules and periportal hepatocyte necrosis
76
Q

what is the subacute phase of suppurative cholangitis/cholangiohepatitis

A
  1. cholangiohepatits with mixed inflammation + bile duct proliferation and variable periportal to bridging fibrosis
77
Q

what is the chronic stage of suppurative cholangitis/cholangiohepatitis

A

concentric periportal fibrosis and pseudolobule formation

78
Q

what is the pathogenesis of suppurative cholangitis/cholangiohepatitis

A

biliary tract inflammation assocaited with ascending bacterial infection

79
Q

what is the most common bacteria involved in suppurative cholangitis/cholangiohepatitis

A

E. coli

80
Q

where are the bacteria present in suppurative cholangitis/cholangiohepatitis

A

portal vessels, sinusiods and parenchyma than the bile ducts

81
Q

what age does lymphocytic cholangitis/cholangiohepatits most common occur in cats

A

>4 years

82
Q

what does lymphocytic cholangitis/cholangiohepatits lead to

A

progression to prominent fibrosis with cholestasis and possible icterus

83
Q

what is gallbladder mucocele in dogs

A

gallbaldder distention with accumulated mucoid secretion

possible extension and accumulation of bile laden mucus into cystic, hepatic and common bile ducts –> variable extrahepatic obstruction

84
Q

what can occur with severe cases of gallbladder mucocele in dogs

A

distention with abnormal semisolid accumulations of mucus

possible ischemic necrosis and rupture

85
Q

what histopathological changes can be seen with gallbladder mucocele

A

hyperplasia of mucus secreting glands

formation of mucus filled cysts

86
Q

what is the etiopathogenesis of gallbladder mucocele (3)

A
  1. decreased gallbladder motility
  2. bile stasis
  3. altered bile compostition and viscosity
87
Q

what breed is juvenile pancreatic atrophy commonly seen in

A

german shepherds

88
Q

what is the etiology of juvenile pancreatic atrophy

A

preceded by intense inflammatory cell infiltration dominated by CD*+ T-lymphocytes (atropic lymphocytic pancreatitis)

presumed autoimmune process against acinar cells

89
Q

what is exocrine pancreatic insufficiency (EPI) caused by in dogs

A

juvenile pancreatic atrophy

90
Q

what is exocrine pancreatic insufficiency (EPI) caused by in cats

A

chronic pancreatitis

91
Q

what occurs with clinical onset of exocrine pancreatic insufficiency

A

85%-90% of secretory capacity is lost

92
Q

how is exocrine pancreatic insufficiency diagnosed

A

serum levels of trypsin like immunoreactivity (TLI)

93
Q

what are the clinical features of exocrine pancreatic insufficiency (3)

A
  1. diarrhea and chronic weight loss despite voracious appetite
  2. possible steatorrhea (fat in feces) due to inadequate digestion and assimilation of lipids
  3. malassimilation of nutrients (lack of direct digestive action of pancreatic enzymes and lack of activation of intestinal enzymatic activities)
94
Q

what is the pathogenesis of acute pancreatic necrosis

A

activation of trypsinogen to trypsin within acinar cells

trypsin then causes activation of pancreatic enzymes which causes autodigestion of the pancreas

95
Q

what are the early lesions in acute pancreatic necrosis

A

necrosis and inflammation at the periphery of affected lobules

with variable involvement of adjacent adipose and connective tissue

96
Q

what do elastase and phospholipase A enzyme activation cause in acute pancreatic necrosis

A

expansion of the area of pancreatic necrosis

97
Q

what do lipases cause in acute pancreatic necrosis

A

hydrolysis and necrosis of peripancreatic fat

98
Q

what are the effects of the acute pancreatic enzymes

A

trypsin, phospholipase A, elastase, lipase and colipase –>

damage the walls of the local blood vessels –>

increased vascular permeability –>

edmea, hemorrhage, thrombosis

99
Q

how is the complement cascade activated in acute pancreatic necrosis (4)

A

the enzymatic tissue necrosis + superimposed ischemic necrosis

  1. local activation of the complement cascade
  2. release of cytokines TNF-alpha, IL-1. IL-6, IL-8 and platelet-activating factor (PAF)
  3. leukocyte chemotaxis into the area
  4. amplification of pancreatic damage via the generation ROS and additional cytokine release
100
Q

what are the systemic effects of acute pancreatic necorsis (7)

A
  1. cytokines, NO and activated digestive enzymes are released into the circulation
  2. consumption of circulating protease inhibitors
  3. activation of kinin system, coagulation, fibrinolytic system, complement
  4. systemic inflammatory response
  5. hypotension
  6. hypovolemic shock
  7. DIC
  8. multiple organ failure
101
Q

what does the release of activated enzymes, vasoactive peptides, inflammatory mediators and embolic debris into the systemic circulation (3)

A
  1. multifocal hepatocellular necrosis
  2. pulmonary edema and acute interstitial pneumonia
  3. myocardial injury with arrhythmias
102
Q

what can lead to acute renal failure from acute pancreatic necrosis

A

microvascular thrombosis in DIC

tubular degeneration induced by hypotension/hypoperfusion

103
Q

what are complications that can occur in acute pancreatic necorsis due to the systemic effects (4)

A
  1. portal vein thrombosis
  2. pulmonary thromboembolism
  3. physical obstruction of the extrahepatic bile duct or duodenum
  4. intestinal ileus (intestinal paralysis)
104
Q

what factors increase the risk for acute pancreatic necrosis (8)

A
  1. middle aged to old dogs
  2. overweight or obese
  3. nutrtitional factors (amount and quality of dietary lipids)
  4. breeds: mini schnauzer, yorkie, mini poodles, non-sporting/non-working breeds
  5. females > males
  6. hyperadrenocorticism
  7. hypothyroidism
  8. hypercalcemia
105
Q

what is acute pancreatitis

A

inflammation with ductal and lobular distribution

106
Q

what is acute pancreatitis in dogs

A

reflux of bacteria or activated enzymes and bile salts from the intestine

107
Q

what is acute pancreatitis in cats

A

frequently associated with Toxoplasmosis

108
Q

what is chronic pancreatitis

A

extension of inflammatory process starting in the ducts

109
Q

what is chronic pancreatitis frequently associated with (3)

A
  1. ascending infection with intestinal bacteria
  2. migration of flukes
  3. migrating larvae of strongylus equinus and strongylus edentatus in horses
110
Q

what causes granulomatous/pyogranulomatous pancreatitis

A

systemic fungal infections

feline infectious peritonitis

111
Q

what are biomarkers used for pancreatitis/pancreatic necrosis (2)

A
  1. canine pancreas-specific lipase (cPSL)
  2. canine pancreatic elastase-1 (cPE-1)
112
Q

what is feline pancreatitis commonly associated with

A

concurrent disease in other organ systems

113
Q

what are frequent co morbidities associated with feline pancreatits

A

hepatic lipidosis

inflammatory liver disease (ILD)

bile duct obstruction

diabetes mellitus

inflammatory bowel disease (IBD)

vitamin deficiencies (B12/cobalamin, folate, K)

intestinal lymphoma

nephritis

pulmonary thromboembolism

pleural and peritoneal effusions

114
Q

what is triaditis

A

concurrent inflammation of the pancreas, liver and small intestine

115
Q

what are the clinical features of triaditis

A

anorexia, weight and muscle mass loss, diarrhea, vomiting, icterus, hepatomegaly, thickened intestine, pancreatic mass, abdominal pain, abdominal effusion, pyrexia, hypothermia, tachypnea, dyspnea and shock

116
Q

what are the clinical chemistry abnormalities in triaditis

A

liver enzymes elevation (ALT, AST< GGT, ALP) + bilirubin increase (hepatobiliary disease)

eleveated pancreatic lipase serum levels (pancreatitis)

decreased cobalamin, folate and albumin (IBD or intestinal lymphoma)

Module 16 (26 decks)

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