Hepatobiliary Flashcards
1
Q
Liver toxins: environment
A
cycad palms
amanita mushroom
aflatoxin
blue-green algae
2
Q
Liver toxin: food
A
xylitol
3
Q
Liver toxin: chemicals
A
heavy metal
arsenic
4
Q
Liver toxins: drugs
A
acetaminophen, amiodarone, azathioprine, carprofen, corticosteroids, diazepam (cat, oral), diethylcarbamazine-oxibendazole, doxycycline, griseofulvin (cat), halothane, ketoconazole, lomustine, mebendazole, methimazole (cat), methotrexate, mitotane, nitrofurantoin, phenazopyridine, phenobarbital, stanozolol (cat), sulfonamides, tetracycline, thiacetarsamide, zonisamide
5
Q
Liver infections: bacterial
A
lepto
mycobacterium tuberculosis
escherichia coli
clostridium perfringens
6
Q
Liver infections: viral
A
canine adenovirus-1
7
Q
Liver infections: fungal
A
blastomyces dermatitis
cryptococcus neoformans
histoplasma capsulatum
coccidioides immitis
8
Q
Liver infections: parasitic
A
platynosomum fastosum
toxoplasmosis
schistosomiasis
migrating larvae
9
Q
when can you see icterus?
A
serum bilirubin > 3 mg/dL (up to 5)
10
Q
when can you see icteric plasma?
A
bilirubin > 0.5-1 mg/dL
11
Q
what is the most common cause of ascites in liver disease?
A
portal hypertension, although decreased vascular oncotic pressure form hypoalbuminemia may play a role
12
Q
causes of prehepatic portal hypertension?
A
increased resistance in extra hepatic portal vein; associated with mural or intraluminal obstruction (congenital atresia or fibrosis, thrombosis, neoplasia) or extraluminal compression; hepatic AV fistula
13
Q
typical signalment & presentation of patient with prehepatic portal hypertension?
A
young
ascites
hepatic encephalopathy
14
Q
causes of intrahepatic portal hypertension?
A
increased resistance in microscopic portal vein tributaries, sinusoids, or small hepatic veins. divided into presinusoidal, sinusoidal, post sinusoidal
ex: chronic hepatitis w/fibrosis or cirrhosis
15
Q
most common cause of intrahepatic portal hypertension?
A
chronic hepatitis with fibrosis or cirrhosis
16
Q
causes of post hepatic portal hypertension?
A
obstruction of larger hepatic veins such as post hepatic caudal vena cava or right atrium. ex) right heart failure, pericardial disease, pulmonary hypertension, Budd-Chiari syndrome
17
Q
what is the protein content in prehepatic portal hypertension
A
low protein (<2.5 g/dL)
18
Q
what is the protein content in pre-sinusoidal portal hypertension
A
low protein (<2.5 g/dL)
19
Q
what is the protein content in post-sinusoidal portal hypertension
A
high protein (>2.5 g/dL)
20
Q
what is the protein content in post-hepatic portal hypertension
A
high protein (>2.5 g/dL)
21
Q
what is the protein content in sinusoidal intra-hepatic portal hypertension
A
could be high or low, more likely high (>2.5 g/dL)
22
Q
toxins implicated in hepatic encephalopathy?
A
ammonia, aromatic amino acids, bile acids, endogenous benzodiazepines, gamma aminobutyric acid, glutamine, phenol, SCFA, tryptophan, decreased alpha-ketoglutarate, false neurotransmitters
23
Q
why might chronic hepatic encephalopathy occur in cats?
A
hepatic lipidosis: cannot synthesize arginine in the liver, and depletion of arginine occurs w/prolonged fasting. arginine is necessary for completion of urea cycle; without it, ammonia detoxification is impaired
24
Q
ALT half-life
A
dog: 48-60h
cat: 6h
25
AST half-life
dog: 22h
cat: 77 min
26
where is AST found?
liver, muscle, RBC
27
where is ALT found?
liver >>> muscle
28
pattern of CK increase after muscle injury
increases quickly, peak levels 6-12 hours post-injury
| half-life is short, so decreases w/in 24-48h post injury
29
how much of AST is in mitochondria?
20%
30
why is AST less sensitive than ALT for detecting hepatic injury?
20% is in mitochondria
| shorter half-life
31
why is AST less specific than ALT for detecting hepatic injury?
found in blood & muscle as well as liver
32
which of the following would cause the biggest increase in ALT? hepatic neoplasia, cirrhosis, hepatocellular necrosis & inflammation, biliary tract dz (obstructive), biliary tract dz (nonobstructive)
hepatocellular necrosis & inflammation
33
in acute liver disease, a decrease of XX% or more of ALT over a few days is considered a good prognostic sign
50%
34
what attaches ALP to cell membranes?
glucosyl phosphatidylinositol linkages
35
which liver enzyme has the lowest specificity for hepatobiliary dz?
ALP
36
in dogs, what is the sensitivity and specificity of ALP for hepatobiliary disease?
sens: 80%. spec: 51%
37
where is ALP found in the dog?
in descending order of how much: intestinal mucosa, renal cortex, placenta, liver, bone
38
plasma half life of L-ALP (dog & cat) & C-ALP (dog)
dog: L & C: 70 hr
cat: L: 6hr
39
in the cat, what is the sensitivity and specificity of ALP for hepatobiliary disease?
sens: 50%
spec: 93%
40
in what feline endocrine disease may B-ALP contribute significantly to elevations in ALP?
hyperthyroidism
41
in dogs, what is the sens & spec of GGT for hepatobiliary dz?
sens 50%, spec 87%
| concurrent incr in ALP increase spec to 94%
42
in cats, what is the sens & spec of GGT for inflammatory liver dz?
sens 86%, spec 67%
43
how can GGT & ALP help differentiate type of liver dz in a cat?
hepatic lipidosis (underlying cause isn't necroinflammatory): ALP relative to upper limit will be greater than magnitude of incr GGT. necroinflam liver dz: incr in GGT of greater magnitude than incr in ALP
44
hypoglycemia occurs after what % of liver function is lost?
75%
| occurs d/t reduction of hepatic glycogen stores, gluconeogenesis, & clearance of insulin
45
hypoalbuminemia occurs after what % of liver function is lost?
70%
46
hyperalbuminemia has been reported in patients with what disease?
hepatocellular carcinoma
47
which globulins is the liver responsible for making?
alpha & beta
| gamma-globulins come from B lymphocytes & plasma cells
48
how does cholesterol help you define type of liver dz?
hypo: end-stage liver dz
hyper: cholestatic liver dz
49
why do you see increase in globulins with PSS or decreased hepatic mass?
decreased filtration & clearance of toxins & microbial agents form portal circulation
50
why is there an increase in bilirubin with sepsis?
cytokines inhibit expression of hepatocyte transporters necessary for bilirubin transport
can occur w/o the presence of hepatobiliary dz
51
you can see hyperbilirubinemia with which artifacts?
hemolysis & lipemia
52
what % of cats with hepatic lipidosis have hyperbilirubinemia?
>95%
53
how might an EHBDO affect feces?
absence of stercobilin = acholic feces
54
what is delta bilirubin?
bile duct obstruction - conjugated bilirubin in plasma binds irreversibly covalently with albumin (delta bilirubin); half-life is 2 weeks = can stay icteric for several weeks despite resolution of bile duct obstruction
55
patients with a congenital PSS are or are NOT likely to be icteric? why?
are NOT: bilirubin is not affected by abnormal liver perfusion.
56
bile acids are synthesized from what?
cholesterol (in the liver)
57
what hormone is the major stimulus for GB contraction? where does it come from? in response to what?
cholecystokinin, from the duodenal mucosa, in response to fat or protein in ingesta
58
what is the process of enterohepatic circulation?
GB contraction -> bile goes from GB to duodenum (to solubilize dietary lipids), then reabsorbed in the ileum & transported back to liver via portal vein, where 95% of bile acids are removed & process starts all over again
59
pre & post prandial bile acids are what % sens/spec for diagnosis of PSS?
99% sens, 95-100% spec
| fasting alone: dog - 93% sens, 67% spec; cat - 100% sens, 71% spec
60
how can lipemia change bile acids?
false increase
61
what clin path abnormality can anorexic cats with liver disease get? why?
hyperammonemia: lack of arginine, which is an essential substrate for detoxification of ammonia in the urea cycle
62
hepatic dysfunction must cause a xx% reduction in urea cycle function in order for hyperammonemia to result
70%
63
sens/spec of elevated fasting ammonia for dx PSS?
sens 98%, spec 89%
64
describe the procedure for an ammonia tolerance test
give 2mL/kg of 5% NH4Cl deep into rectum. measure ammonia pre- & 20 & 40min post-administration
65
liver produces which clotting factors?
all except the von willebrand subtype of factor VIII
66
how does cholestasis affect clotting?
causes malabsorption of fat-soluble vitamins (ie vitamin K)
67
which are the Vet K dependent clotting factors?
2 7 9 10 protein C protein S
68
most common coagulation abrnomality in cats with hepatobiliary dz?
increased PT
69
which clotting inhibitory proteins are produced in the liver?
antithrombin III, protein C, protein S
70
what is hypersplenism? it occurs secondary to what disease?
splanchnic pooling of blood can lead to prolonged capturing of platelets at their degradation site in the spleen -> thrombocytopenia
occurs secondary to portal hypertension
71
coag parameters associated with DIC?
low fibrinogen
thrombocytopenia
prolonged PT & aPTT
elevated FDP & D-dimers
72
what is protein C?
```
disulfide-linked glycoprotein
molecular weight similar to albumin
synthesized in liver
circulates as plasma zymogen
once activated, binds protein S -> together they exert anticoagulant effects by degrading factors Va & VIIIa
```
73
half life of protein C
6 hours
74
protein C less than XX% is common in patients with PSS but rare in MVD
70% (seen in 88% of PSS, 5% of MVD patients)
75
what CBC abnormalities are commonly seen with hepatic disease?
microcytosis (associated with impaired iron transport in patients with vascular abnormalities),
target cells,
poikilocytosis,
heinz body formation (cats),
anemia d/t hemorrhage from GI ulceration / coag disorder / anemia of chronic dz,
+/- mild thrombocytopenia
76
what UA finding in cats is specific for liver disease?
bilirubinuria (can also be seen with hemolytic dz)
77
why can dog urine have bilirubin in it normally?
low renal threshold for bilirubin excretion, and kidneys have enzymes needed to produce bilirubin from heme & to conjugate it
78
what crystals can be found in urine of dogs & cats with PSS? why?
ammonium biurate
due to reduced conversion of uric acid to allantoin & of ammonia to urea. ammonia & uric acid aggregate in acidic urine to form crystals
79
what breeds are associated with developing ammonium biurate crystals w/o hepatobiliary dz?
dalmation
english bulldog
possibly siamese cats
80
what UA finding might a patient with copper storage hepatopathy have?
fanconi-like: glycosuria w/normal BG, +/- proteinuria
| due to copper accumulation in renal tubules
81
why do patients with hepatobiliary dz have a low USG?
loss of renal medullary hypertonicity d/t low BUN
impaired hormone metabolism: decreasing cortisol metabolism -> Cushing's-like syndrome
psychogenic polydipsia
82
measurements from what imaging modality & view has the highest correlation with actual liver weight in dogs?
measuring right lateral abdominal radiographs
83
discuss CT versus AUS for diagnosis of PSS
CT-angio: sens 96%, spec 89%
| CT-angio is 5.5x more likely to correctly determine presence/absence of cPSS than AUS
84
discuss technetium for diagnosing PSS
Tc-sulfur colloid: colloidal particles that localize in reticuloendothelial system. normal dogs - localize in liver. PSS - localize in lung. not specific for PSS. cats - lung uptake is normal
85
discuss per-rectal portal scintigraphy
normal - pertechnetate goes liver -> heart. PSS: bypass liver; goes to heart first.
86
trans-splenic portal scintigraphy: describe path of uptake
normal: spleen - splenic vein - left gastric vein - main portal vein - liver - hepatic sinusoids - hepatic vein - caudal vena cava - heart
can distinguish between portoazygous & portocaval/splenocaval shunts
87
what is glutathione?
tripeptide synthesized from L-glutamate, L-cysteine, & glycine
essentail antioxidant
stored in hepatocytes
88
why should care be exercised when giving stored RBC to dogs/cats with acute liver injury
ammonia concentrations can increase during storage
89
why are patients with acute liver injury sometimes vitamin K deficient?
cholestasis
90
where is copper found in primary copper hepatopathy?
centrilobular zone of liver
91
where is copper found in secondary copper hepatopathy? why does it accumulate?
periportal zone of liver; secondary to cholestasis
92
what is the pathophysiology of hepatic fibrosis?
chronic hepatic inflammation leads to activation of myofibroblasts including hepatic stellate cells & portal fibroblasts, which cause hepatic fibrosis. oxidative injury can also lead to hepatic stellate cell activation
93
what are the 4 groups of cholangitis, according to WSAVA?
neutrophilic, lymphocytic, destructive, and chronic cholangitis associated with liver fluke infestation
94
causes of acute canine hepatitis: infectious
canine adenovirus-1, leptospirosis, clostridium, canine monocytes ehrlichiosis (E canis)
95
causes of acute canine hepatitis: toxins
mycotoxin, aflatoxicosis, cyanobacteria (microcystin toxicosis - blue green algae), amanita mushrooms, xylitol, manganese overdose (joint supplement), alpha lipoid acid, organic solvents (CCl4)
96
causes of acute canine hepatitis: drugs
carprofen, acetaminophen, TMS, azathioprine, amiodarone, mitotane
97
symptoms of CAV-1
fever, lethargy, anorexia, cranial abdominal pain, melon, vomiting, diarrhea, chem - liver & kidney involvement, bronchopneumonia, conjunctivitis, photophobia, corneal opacity / blue eye d/t anterior uveitis & corneal edema
98
most commonly recognized infectious cause of acute hepatitis in dogs?
leptospirosis (interrogans or kirschneri)
99
how can you definitively diagnose amanita mushroom ingestion?
alpha-amanitin can be detected in liver tissue by liquid chromatography-mass spectrometry
100
In dogs and cats with hepatic inflammation, what are the 5 most common organisms cultured from bile?
E coli, enterococcus, bactericides, streptococcus, clostridium
101
which copper oxidation state is responsible for most of copper's hepatotoxicity?
cupric (Cu2+)
102
what does COMMD 1 stand for?
copper metabolism gene MURR1- containing domain 1
103
name two copper-specific stains
rubeanic acid &rhodamine
104
why shouldn't you give D-penicillamine and zinc concurrently?
D-pen will chelate zinc in the blood, reducing its effectiveness
105
what % of feline liver biopsies reveal inflammatory disease?
26% (45 of 175)
106
what is the most common liver disease in cats?
hepatic lipidosis
107
what is the proposed pathogenesis of neutrophilic cholangitis?
ascending intestinal bacterial infection
108
what is the most common liver enzyme affected in cats with cholantigis?
AST (98% have increase); ALT: 50-57% have increase, ALP incr in 14-48%, GGT variable; about 2/3 are hyperbilirubinemic
109
what test has higher specificity than enzymatic testing for liver dz?
pre- and post-prandial bile acids
110
discuss agreement between cytology & histopathology of feline liver
overall 51% agreement. inflammatory dz correctly diagnosed in 27%. vacuolar hepatopathy correctly diagnosed in 83%. Lymphoma may be misdiagnosed as hepatic lipidosis.
111
what is the most common organism in bile cultures?
E coli
112
What is the most common biochemical abnormality in cats with lymphocytic cholangitis?
hypergammaglobulinemia
113
which has a better prognosis? neutrophilic or lymphocytic cholangitis?
lymphocytic (795d versus about 1y)
114
what % of cats with solitary hepatic abscesses have polymicrobial infection?
>50%
115
what are the intermediate / paratenic hosts for platynosomum?
lizards, terrestrial snails, isopods
116
what is platynosomum?
liver fluke
117
treatment for platynosomum?
praziquantel
118
when does a cat not shed platynosomum eggs?
complete bile duct obstruction
119
what is the fetal vessel that bypasses the hepatic circulation?
ductus venosus
120
what initiates closure of the ductus venosus?
blood pressure changes after umbilical venous flow ceases; thromboxane or various adrenergic compounds stimulate contraction of musculature of ductus venosus & may aid in vessel's closure
121
what are the two main trophic hormones for hepatic growth? (i.e. the ones that the liver doesn't get in a PSS)
insulin & glucagon
122
what toxins are implicated in hepatic encephalopathy?
ammonia; decreased alpha-ketoglutaramate; glutamine; aromatic amino acids; SCFA; false neurotransmitters (tyrosine/octopamine, phenylalanine/phenylethylamine, methionine/mercaptans); tryptophan; phenol (from phenylalanine & tyrosine); bile acids; gamma-aminobutyric acid (GABA); endogenous benzodiazepines
123
what is the proposed mechanism of hepatic encephalopathy for ammonia?
increased brain tryptophan & glutamine; decreased ATP availability; increased excitability; increased glycolysis; brain edema; decreased microsomal Na-K-ATPase in brain
124
what is the proposed mechanism of hepatic encephalopathy for decreased alpha-ketoglutaramate?
diversion from Kreb's cycle for ammonia detoxification; decreased ATP availability
125
what is the proposed mechanism of hepatic encephalopathy for glutamine?
alters blood-brain barrier amino acid transport
126
what is the proposed mechanism of hepatic encephalopathy for aromatic amino acids?
decreased DOPA neurotransmitter synthesis; altered neuroreceptors; increased production of false neurotransmitters
127
what is the proposed mechanism of hepatic encephalopathy for SCFA?
decreased microsomal Na,K-ATPase in brain; uncouples oxidative phosphorylation, impairs oxygen utilization, displaces tryptophan from albumin, increasing free tryptophan
128
what is the proposed mechanism of hepatic encephalopathy for false neurotransmitters?
tyrosine -> octopamine; phenylalanine -> phenylethylamine; methionine -> mercaptans. impair norepinephrine action, synergistic with ammonia & SCFA; decrease ammonia detoxification in brain urea cycle; GIT-derived (fetor hepaticas - breath odor in HE); decreased microsomal Na,K-ATPase
129
what is the proposed mechanism of hepatic encephalopathy for tryptophan?
directly neurotoxic; increases serotonin: Neuroinhibition
130
what is the proposed mechanism of hepatic encephalopathy for phenol (from phenylalanine & tyrosine)
synergistic with other toxins; decreases cellular enzymes; neurotoxic & hepatotoxic
131
what is the proposed mechanism of hepatic encephalopathy for bile acids?
membranocytolytic effects alter cell/membrane permeability; blood-brain barrier more permeable to other HE toxins; impaired cellular metabolism d/t cytotoxicity
132
what is the proposed mechanism of hepatic encephalopathy for gamma-aminobutyric acid
(AKA GABA) neural inhibition: hyperpolarizes neuronal membrane; increase blood-brain barrier permeability to GABA
133
what is the proposed mechanism of hepatic encephalopathy for endogenous benzodiazepines?
neural inhibition: hyper polarize neuronal membrane
134
what % of hepatic blood & oxygen is provided by the portal vein? where does the rest of it come from?
80% of the blood and 50% of the oxygen; rest from hepatic arterial blood
135
what is the flow of blood through the liver?
portal vein -> branches -> venues -> portal triad -> hepatic sinusoids -> reticuloendothelial system -> central veins -> hepatic venues -> hepatic vein -> CVC
136
what are the three most common causes of acquired extra hepatic shunts?
hepatic fibrosis/cirrhosis, PVH with portal hypertension, HAVMs
137
what % of cats & dogs with PVH have concurrent congenital macroscopic PSS?
58% of dogs, 87% of cats
138
what % of liver function is lost when hepatic encephalopathy occurs?
70%
139
top breeds for congenital EHPSS?
yorkie, maltese, havanese, dandie dinmont terrier, pug, mini schnauzer
140
what is the odds ratio for Yorkies & PSS?
35.9x greater than all other breeds combined
141
why are dogs with PSS PU/PD?
poor medullary concentration gradient from low BUN, increased renal blood flow, increased ACTH secretion & associated hypercortisolism, psychogenic polydipsia from HE
142
ascites occurs in what % of dogs with HAVM?
75%
143
what % of cats with PSS show ptyalism?
75%
144
GI hemorrhage is more common in dogs with IHPSS or EHPSS?
IHPSS
145
why do dogs/cats with PSS form ammonium urate calculi?
decreased urea production, increased ammonia excretion, decreased uric cid metabolism
146
CNS signs are most frequent with which PSS formation?
splenocaval CPSS
147
at what age are most pets diagnosed with HAVM?
within the first year of life
148
what % of dogs with HAVM have ascites?
75%; we suspect that acquired shunts lead to decompression of the portal system in the remaining 25%
149
what is the typical erythrogram in dogs/cats with PSS?
mild to moderate, microcytic, normochromic, non regenerative anemia; target cells in dogs & poikilocytes in cats
150
why do animals with PSS have RBC microcytosis?
defective iron-transport mechanism, decreased serum iron concentrations, decreased TIBC, increased hepatic iron stores in Kupffer cells; iron sequestration?
151
what are the typical ALT & ALP in dogs with PSS?
increased 2-3x normal; ALP > ALT
152
what serum biochemical changes do you typically find in animals with PSS?
low albumin, low BUN, low cholesterol, low BG, high ALT, high ALP, low creatinine
153
what is the theory behind why proteinuria is common in dogs with PSS?
glomerulopathy (glomerular sclerosis, glomerulofibrosis, membranoproliferative glomerulonephritis): accumulation of antigens reaching the kidneys that the liver would have otherwise cleared with a normal portal circulation -> immune-med GN
154
what is the basic pathway of bile acids?
synthesized in liver from cholesterol -> conjugation -> secreted in bile canaliculi & stored in GB until release into duodenum. aid in lipid absorption via intestinal fat emulsification & metabolism. reabsorbed in ileum -> transported in portal system -> extracted by hepatocytes for recirculation
155
what dog breed can have elevated serum bile acids w/o evidence of hepatocellular dysfunction?
maltese
156
what enzyme deficiency in cats can cause hyperammonemia & HE?
ornithine transcarbamylase, leading to error in ammonia metabolism in urea cycle
157
describe PT and PTT in patients with acute versus chronic liver disease?
chronic - prolonged PTT. acute - prolonged PT & PTT
158
How can plasma protein C activity help differentiate between MVD & PSS?
protein C levels are >70% in 88% of dogs with MVD & low in dogs with PSS
159
what electrolyte abnormality can contribute to HE?
hypokalemia
160
what acid-base abnormality can contribute to HE?
metabolic acidosis
161
why is vegetable protein preferred to animal protein for diets for PSS dogs?
vegetable proteins have less aromatic amino acids (tyrosine, phenylalanine) & more branched chain AA (valine, leucine, isoleucine)
162
what are the prognostic indicators for medical management of dogs with CPSS?
age at onset of c/s (longer survival for older dogs); BUN (longer survival with higher value)
163
what % of dogs treated medically for a CPSS could be expected to be euthanized w/in 10 mo's of diagnoses?
>50%
164
what % of dogs with CPSS can survive long term w/medical management alone?
33%
165
in anesthesia for dogs with liver disease, what characteristics of drugs should be avoided?
avoid anesthetic agents that are highly protein-bound or dependent on liver metabolism
166
what % of EHPSS & what % of IHPSS dogs tolerate complete shunt ligation?
EHPSS: 32-52%. IHPSS: <15%
167
symptoms of acute portal hypertension? (such as with complete ligation of a PSS)
ascites, intestinal congestion, diarrhea, hypoxemia, bowel death
168
following temporary shunt attenuation, intraoperative portal pressures >XX cm water above resting (preligation) pressures or absolute pressures >XX cm water have been associated with greater postoperative complications
>9-10 cm above resting; >17-24 cm water absolute
169
surgical complication rates are higher with IHPSS or EHPSS?
IHPSS
170
what are the more worrisome c/s after a shunt ligation?
vomiting, abdominal distension, progressive ascites, abdominal pain, hypotension; can lead to shock and DIC
171
most common long-term complication seen after surgical treatment of PSS?
recurrence or persistence of c/s
172
what additional complication do IHPSS dogs have that EHPSS dogs don't?
severe GI ulceration & bleeding
173
how are feline PSS management and canine different?
cats have higher preoperative complication rates & worse long-term outcomes
174
what artery to HAVM typically form from?
hepatic artery; but have also been reported to involve gastroduodenal artery, left gastric artery, phrenic arteries
175
how common are MAPSS in dogs with HAVM?
they have been reported in every dog with HAVM
176
what are the treatments for HAVM?
liver lobectomy, ligation of nutrient artery, fluoroscopically-guided glue embolization of abnormal arterial vessels
177
return of bile acids to normal after PSS attenuation is or is not correlated with long-term outcome?
is NOT
178
hepatic vascular anomalies: prognostic indicator for medical management alone?
age at onset of c/s, BUN
179
most common cause of death after PSS attenuation?
severe persistent neuro signs; other causes - intra-op hemorrhage, post-op coagulopathy, portal hypertension, hemorrhagic gastroenteritis
180
dogs undergoing surgery for EHPSS: prognostic indicators?
hypoalbuminemia (in dogs undergoing aneroid constrictor placement) = more likely to have persistent post-op shunting. other factors: pre-op hypoalbuminemia, leukocytosis, seizures after surgery, persistent shunting 6-10 wks after surgery = poor long-term prognosis
181
MST for IHPSS?
1-3 years. post-op complications as high as 77% w/surgery, short-term mortality 11-28%. overall mortality 23-64%.
182
IHPSS: prognostic indicators
better short-term outcomes: body weight >10kg, total protein >4g/dL, albumin >2.6 g/dL, BUN >7.4g/dL. better long-term survival w/higher PCV & TP. Poorer long-term outcome w/pre-op hypoalbuminemia or leukocytosis, seizures after sx, persistent shunting 6-10 wks after sx. Note: post-op serum bile acids have NOT been associated with survival
183
MVD/PVH: survival %?
92% have had good long-term survival
184
most common post-op complications in cats undergoing sx for PSS?
neuro dysfunction, including generalized seizures & central blindness, which can resolve a few months after surgery
185
what is the most common predominantly secondary metabolic hepatopathy in small animals?
vacuolar hepatopathies
186
define vacuolar hepatopathies
a condition in which hepatocytes become loaded with fat (steatosis) or glycogen or water (hepatocellular swelling, or cloudy swelling); lysosomal storage diseases can also lead to hepatocyte vacuolation
187
what causes cloudy swelling? what are the consequences?
occurs when hepatocytes are injured & less able to maintain fluid homeostasis; if swelling is severe & chronic, it can cause hepatocyte death, fibrosis, and cirrhosis
188
severe congenital cobalamin deficiency has been reported to cause what liver change(s) in dogs? why do we think this occurs?
foamy vacuolation of hepatocytes, lipogranulomas, single cell necrosis, & mild fibrosis; possibly due to secondary hyperhomocysteinemia
189
vacuolar hepatopathy can lead to what cancer in what breed? what lab work change do you see associated with this?
HCC in scottish terriers. increased ALP
190
what vitamin deficiency can lead to steroid hepatopathy & cloudy changes in dogs?
cobalamin deficiency
191
what endocrine diseases in cats & dogs can lead to steatosis?
dogs: hypothyroidism, DM. cats: hyperthyroidism
192
name two toxic causes of vacuolar hepatopathies
aflatoxin (dogs), vitamin A (cats)
193
describe the process of steroid hepatopathy development
hepatocytes become vacuolated with marked cytoplasmic, or even nuclear, increases in glycogen. vacuolation starts in the centrilobular region (zone 3) & become generalized when chronic
194
why do dogs get an increase in ALP with steroid hepatopathy?
could be a result of delayed clearance of the intestinal isoenzyme d/t hyperglycosylation in the liver under the influence of GCC
195
what is the treatment for steroid hepatopathy?
remove the source of exogenous/endogenous GCC. if that isn't possible, antioxidants (SAMe increases hepatic glutathione & had beneficial effect on oxidized:total glutathione ratio in hepatocytes)
196
what is the typical signalment of a scottie with idiopathic vacuolar hepatopathy?
middle-aged (median 8y, although dogs with HCC are older); no gender predilection
197
describe lab work abnormalities & c/s in scotties with idiopathic vacuolar hepatopathy?
moderate to marked elevation in ALP and milder increase in ALT; nearly half show c/s suggestive of hyperadrenocorticism, but ACTH stim & LDDST are variable
198
what are the most consistent endocrine abnormalities in scotties with idiopathic vacuolar hepatopathy?
increases in progesterone & androstenedione post-ACTH stimulation
199
what is the difference between macrovesicular and microvesicular steatosis?
micro vesicular - multiple vacuoles that are smaller than the cell nucleus, typical in DM in dogs. macro vesicular - larger vacuoles, which often displace nucleus to periphery of cell. Feline hepatic lipidosis is assoc w/both micro & macro
200
aflatoxicosis causes what metabolic change in the liver?
steatosis (as a result of hepatocyte injury)
201
what changes occur to the liver cells in chronic vitamin A intoxication in cats?
hypertrophy of lipid-laden hepatic stellate cells, with or without hepatocellular steatosis & fibrosis
202
what metabolic change can be seen in livers of dogs with congenital PSS?
steatosis
203
name 3 predisposing factors for feline hepatic lipidosis
obesity, anorexia, stress
204
how much weight do cats have to lose to develop feline hepatic lipidosis?
25? in one study, 30-40% in another
205
describe the proposed pathophys of feline hepatic lipidosis
fasting + stress = increase in peripheral lipolysis -> bottleneck effect in liver, such that mobilized lipids become trapped, with reduced export. marked steatosis of hepatocytes interferes with metabolic activity of cells and produces a secondary cholestasis d/t compression of small intrahepatic cholangioles. this leads to acute liver failure.
it has also been proposed that protein deficiency and negative nitrogen balance assoc w/fasting reduce ability to produce apoproteins to export fat from liver, and that taurine and carnitine deficiencies contribute to pathogenesis (but these have limited support w/research)
206
describe lipid levels in cats with hepatic lipidosis
elevated circulating triglycerides and NEFA, consistent with lipolysis of peripheral fat & reduced function of HSL; they can also have higher serum beta-hydroxybutyrate than normal cats, indicating hepatic ketogenesis; can still mobilize triglycerides form liver - significant increase in serum VLDL. it's proposed that they can't remove triglycerides fast enough to compensate for increased mobilization
207
insulin in cats with hepatic lipidosis is increased or decreased
normal or reduced (suggesting that affected cats are not insulin-resistant)
208
adiponectin and leptin are high or low in cats with hepatic lipidosis
both are high. high leptin should lead to reduction of lipid content of non-adipose tissues like liver, so affected cats must be leptin-resistant
209
what is the typical signalment of a cat with hepatic lipidosis
younger to middle-aged female cat. idiopathic cases tend to be younger than secondary cases
210
how do you diagnose hepatic lipidosis?
biopsy
211
what are the typical biochem changes in cats with hepatic lipidosis?
marked increase in bilirubin, ALP, ALT; normal GGT (although cat with secondary FHL can have very elevated GGT if there is concurrent biliary stasis). hypokalemia d/t anorexia and vomiting. hyperglycemia
212
what proportion of cats with hepatic lipidosis have prolonged coagulation times
about half; clinically significant bleeding is rarely reported
213
what is the most important factor affecting prognosis in cats with hepatic lipidosis?
early intensive feeding (primary and secondary FHL)
214
what type of diet is most effective at reducing hepatic lipid?
high protein diet
215
what vitamin should be measured in cats with hepatic lipidosis?
cobalamin
216
some cats with hepatic lipidosis develop hepatic encephalopathy. what is the feeding recommendation in this case?
NOT low protein diet, but instead reduce the amount fed - feed in small frequent meals and institute therapies for any concurrent inflammatory disease
217
superficial necrolytic dermatitis has been associated with what drug?
phenobarbital
218
superficial necrolytic dermatitis has been associated with what 2 neoplasms?
glucagonoma, insulinoma
219
describe the pathogenesis of skin lesions associated with superficial necrolytic dermatitis
amino acid deficiency; zinc and fatty acid deficiencies also implicated. these are proposed to be d/t unregulated hepatic metabolic activity under stimulus of increased glucagon activity, or to unidentified stimulus
220
describe the typical signalment of a dog with superficial necrolytic dermatitis
older small-breed dog. 75% male; mean/median 10yo (range 5-15y)
221
describe the skin lesions of superficial necrolytic dermatitis
hyperkeratotic erythematous crusting; on extremities (paw pads, nose, periorbital, perianal), around genitals, pressure points. lesions develop fissures and bacterial infection, painful
222
what % of dogs with superficial necrolytic dermatitis have diabetes mellitus?
25-40%
223
describe histopathology of skin biopsies for superficial necrolytic dermatitis
parakeratotic hyperkeratosis with inter- and intra-cellular edema = red, white, and blue on H and E staining
224
what disease has the same skin histopath lesions as superficial necrolytic dermatitis?
zinc responsive dermatosis
225
describe the treatment for superficial necrolytic dermatitis
supportive care - amino acids, NOT hepatic diet. high-quality, digestible, high-protein diet like those designed for GI dz or convalescence. supplementation with Zn and EFA, egg yolks, antibiotics for skin +/- shampoo, analgesia; avoid steroids
226
what is hemochromatosis?
iron overload in the liver
227
why does secondary hemochromatosis develop?
iron is not excreted in bile. 2ndary dz will occur if there is increased absorption in intestine, abnormal excretion, or increased hepatic storage secondary to red cell hemolysis
228
in hemochromatosis, describe liver lesions
loading of macrophages & Kupffer cells with hemosiderin, hepatocellular degeneration, periportal fibrosis leading to bridging fibrosis and cirrhosis
229
how do dogs develop secondary hemochromatosis?
dietary iron overload, hemolytic anemia d/t pyruvate kinase deficiency, repeated therapeutic blood transfusions
230
what is alpha-1 anti-trypsin?
neutrophil elastase manufactured in liver
231
discuss the 3 forms of alpha-1 anti-trypsin in dogs
fast, intermediate, slow. intermediate - most common in Cockers with chronic hepatitis
232
what is fecal alpha-1 anti-trypsin used for?
detecting protein-losing enteropathy
233
what is serum amyloid a?
acute phase protein made by hepatocytes. its transcription is regulated by cytokines. it is the most common form of amyloid in small animals; usually occurs secondary to inflammatory disease
234
what APP(s) is/are produced in largest amount(s) in the face of inflammation?
SAA & CRP
235
describe amyloid AL
monoclonal IgG light chain. amyloidosis d/t amyloid AL is rare in small animals, but has been described in association with tracheal disease and extra medullary plasmacytoma in dogs and cats. liver involvement is not important with amyloid AL
236
hepatic amyloidosis is most common in which species
cats
237
describe amyloidosis in cats
most commonly familial and systemic (associated with SAA), but can be sporadic. in abyssinians, it usually presents as CKD, with renal medulla involved more than glomeruli. siamese often have hepatic involvement.
238
why do cats with hepatic amyloidosis most often present?
acute intra-abdominal bleeding from fracture of a fixable liver
239
describe the typical clfinicopathologic findings in cats with hepatic amyloidosis
high ALT, globulins, bilirubin; anemia; biliary enzymes rarely increased. may see signs of chronic inflammatory dz / comorbidities
240
if you were to treat a dog with hepatic amyloidosis, what would you use?
colchicine
241
what are the predominant c/s of lysosomal storage diseases?
neurological & skeletal > hepatic
242
what is the predominant c/s in lipid storage disease (cholesterol ester storage disease)
hepatosplenomegaly d/t accumulation of lipid and cholesterol crystals in liver and spleen
243
what are the two major causes of drug-induced hepatotoxicosis?
cytotoxic & cholestasis
244
describe the cytotoxic category of drug-induced hepatotoxicosis
due to hepatocyte toxicosis from parent compound or a locally generated metabolite; leads to a hepatocellular pattern of liver injury d/t hepatocyte necrosis
245
describe the cholestatic category of drug-induced hepatotoxicosis
can occur when compounds inhibit or down regulate transporter pumps in sinusoidal or canalicular membranes, thus interfering with bile salt efflux & hepatocyte functions. cholestatic pattern can also result from mitochondrial injury leading to steatosis
246
list 14 drugs involved in dosage-dependent hepatotoxicosis
acetaminophen, aflatoxin, amanita mushrooms, amiodarone (dog), azathioprine (d), azoles, CCNU (d), cycads (d), glipizide (cat), phenazopyridine (rhabdomyolysis predominates), phenobarbital (d), phenytoin (d), primidone (d), xylitol (d)
247
what are the 4 mechanisms of dose-dependent hepatotoxicity?
oxidative stress, mitochondrial dysfunction, transporter dysfunction, p450 induction
248
describe the "transporter dysfunction" mechanism of dose-dependent hepatotoxicity & give 2 examples
drugs can inhibit or down regulate transporter pumps and lead to a functional cholestasis. Ex) cholestasis of pregnancy (endogenous hormone metabolites), endotoxin
249
describe the "oxidative stress" mechanism of dose-dependent hepatotoxicity & give 3 examples
metabolites cause oxidative stress; antioxidant supplementation may be effective for treatment/prevention of liver toxicosis. ex) acetaminophen, azathioprine, azole antifungals
250
describe the "mitochondrial dysfunction" mechanism of dose-dependent hepatotoxicity & give 2 examples
drugs interfere with mitochondrial function and can lead to steatosis from inhibition of fatty acid beta-oxidation, or can lead to more severe hepatocellular damage due to impaired cellular respiration. ex) tetracyclines, amiodarone
251
describe the "P450 induction" mechanism of dose-dependent hepatotoxicity & give 2 examples
drugs act as P450 inducers and lead to hepatotoxicosis by chronic bioactivation of environmental toxins. ex) phenobarbital, phenytoin
252
describe the theory behind idiosyncratic hepatotoxicity
caused by reactive metabolites that are variably generated among individuals. these metabolites may cause oxidative stress, mitochondrial damage, or lead to formation of haptens that trigger a humoral or T cell-mediated immunologic response. they may or may not involve an adaptive immune response. metabolites may bind to critical proteins and impair hepatocyte function, or generate ROS that damage hepatocyte membranes. drug-protein adducts can be processed and presented to immune system with MHC molecules, which leads to clonal expansion of drug-specific T cells +/- generation of drug-specific antibodies that target hepatocyte proteins. usually requires discontinuation of suspect drug & structurally related drugs.
253
List 6 drugs associated with idiosyncratic hepatotoxicity
carprofen (d), diazepam (c), mitotane (d), potentiated sulfonamides (d), zonisamide (d)
254
in idiosyncratic hepatotoxicityy, how are reactive metabolites generated?
locally in the liver by cytochrome p450s (CYPs), flavin mono-oxygenates (FMOs), or other pathways
255
name two drugs that are associated with idiosyncratic hepatotoxicity via oxidative stress
methimazole and (possibly) diazepam
256
name three drugs that are associated with idiosyncratic hepatotoxicity via drug happen formation with immune response
potentiated sulfonamides, (possibly) felbamate, and (possibly) zonisamide
257
high doses of acetaminophen cause what toxicities?
acute centrilobular hepatic necrosis; cats also get hematologic toxicosis - methemoglobinemia and cyanosis
258
why are cats more susceptible to acetaminophen toxicity?
absent expression of UGT1A6, the enzyme that glucuronidates acetaminophen, and possibly also due to decreased expression of ABCG2 transporter, which exports acetaminophen sulfate in humans
259
why do we treat acetaminophen toxicity with NAC?
acetaminophen is bioactivated to the reactive metabolite, NPQI (N-acetyl-p-benzoquinone imine), which is detoxified by glutathione conjugation. NAC is a glutathione precursor.
260
for animals with methemoglobinemia from acetaminophen intoxication, what drug can be used to restore functional hemoglobin?
ascorbate (vitamin C) (efficacy not evaluated)
261
what is the proposed mechanism of phenobarbital hepatotoxicity?
induction of cytochrome P450 enzymes, which secondary bioactivation and hepatotoxicity of other drugs, dietary components, or environmental toxins.
262
describe phenobarbital hepatotoxicity in cats
phenobarbital does not lead to enzyme induction or hepatotoxicosis in cats
263
discuss the mechanism of ketoconazole hepatotoxicity
oxidative metabolite (N-deacetyl ketoconazole) leads to covalent binding to liver proteins and glutathione depletion; so co-treatment with glutathione precursors like SAM-e can be considered if dogs get increased liver enzymes during treatment
264
discuss the mechanism of azathioprine hepatotoxicity
generation of oxidative metabolites and depletion of hepatic antioxidants; can be prevented by pre-treatment with NAC. oxidative metabolites of azathioprine are generated by xanthine oxidase
265
what breed seems to be more at risk for azathioprine hepatototixcosis?
GSD
266
describe the clin path changes seen with amiodarone toxicity
increases in ALT +/- hyperbilirubinemia, +/- neutropenia
267
discuss the mechanism of amiodarone hepatotoxicity
two oxidative metabolites: mono-N-desethylamiodarone (MDEA), and di-N-desethylamiodarone (DDEA), which generate ROS that uncouple oxidative phosphorylation and lead to mitochondrial damage. these metabolites are generated by CYP3A4 in humans, and their generation can be inhibited by ketoconazole in vitro
268
what breed is most prone to hepatotoxicosis with CCNU? what age?
boxers; younger dogs (<5yo)
269
what should be given concurrently with CCNU in all treated dogs?
denamarin (silybin + SAM-e)
270
discuss the mechanism of tetracycline hepatotoxicity
inhibition of beta-oxidation of fatty acids in hepatic mitochondria, as well as inhibition of hepatic lipoprotein secretion. although tetracycline inhibits fatty acid beta-oxidation in vitro, there is no histologic evidence for steatosis from tetra/doxycycline use in dogs
271
describe clin path changes associated with potentiated sulfonamide hepatotoxicity
hepatocellular pattern progresses over several days to cholestatic
272
what is the most common histologic finding seen with potentiated sulfonamide hepatotoxicity
hepatic necrosis
273
list ADE for potentiated sulfonamides
hepatic necrosis, fever, neutropenia, thrombocytopenia, hemolytic anemia, polyarthropathy, proteinuria, KCS, skin lesions, uveitis
274
discuss the mechanism of potentiated sulfonamide hepatotoxicity
oxidized to form nitroso metabolite that covalently bind to proteins and act as haptens
275
discuss the mechanism of methimazole hepatotoxicity
incr ALT, dose-dependent centrilobular hepatic necrosis, glutathione depletion. oxidative metabolite, N-methylthiourea, is generated by flavin mono-oxygenates
276
aflatoxins are produced by what species?
aspergillus
277
where can aflatoxins be found?
moldy corn, peanuts, or soy; contaminated pet food; wild bird seed
278
describe the mechanism of aflatoxin hepatotoxicosis
aflatoxin B1 is a dose-dependent hepatotoxin. it is bioactivated by cytochrome P450 enzymes to electrophilic epoxide metabolites that lead to protein and DNA adducts and glutathione depletion
279
describe clin path change seen in aflatoxin hepatotoxicosis
decreases in serum protein C, antithrombin, and cholesterol are more sensitive than increases in liver enzymes or bilirubin early in course of disease; hyperbilirubinemia, hypoalbuminemia, and hypocholesterolemia are poor prognostic indicators.
280
what is unique about aflatoxin hepatotoxicosis in dogs, histologically speaking?
massive hepatic necrosis is NOT a feature. rather, you see diffuse hepatocyte lipid vacuolation, fibrosis, biliary hyperplasia +/- cirrhosis
281
how can you test for aflatoxin toxicosis?
submit food for aflatoxin B1 analysis; vomitus, serum, and urine can be analyzed for M1 metabolite of aflatoxin B1
282
describe the progression of toxicosis from xylitol
30-60 minutes: insulin release and hypoglycemia. 6-72 hours: acute hepatic necrosis, sometimes leading to consumptive coagulopathy and fulminant liver failure
283
describe the mechanism of amanita mushroom hepatotoxicosis
amatoxins, especially alpha-amanitin, inhibit RNA polymerases, leading to decreased mRNA generation, arrested protein synthesis, and necrosis of metabolically active cells, including intestinal rapt cells, hepatocytes, and renal tubular cells
284
describe the clinical course of toxicosis from amanita
vomiting/hematochezia/abodminal pain 6-24 hours after ingestion. hypoglycemia 24-48h d/t insulin release stimulated by alpha-amanitin. massive hepatic necrosis and renal tubular necrosis develop after 36-84 hours
285
what drug can be used in amanita toxicosis?
silybin (from milk thistle) inhibits amatoxin uptake by hepatocytes, which is mediated by OATP1B3 transporter
286
how can you diagnose amanita toxicosis
measure alpha-amanitin in urine, serum or plasma, kidney, or liver
287
what genera of blue-green algae cause hepatotoxicosis?
microcystis aeruginosa (freshwater lakes, ponds, reservoirs) and nodularia spumigena (brackish and ocean waters)
288
discuss the mechanism of blue-green algae hepatotoxicosis
cyanotoxins microcystin and nodular inhibit serine/threonine protein phosphates in the liver, with subsequent hyperphosphorylation and disruption of cytoskeletal proteins. this leads to hepatocyte dissociation, hepatic necrosis, and glutathione depletion
289
nodularin can cause disease in what organ other than the liver?
kidney: proximal renal tubular necrosis and anuric kidney injury
290
how can you diagnose blue-green algae toxicosis?
cytology of vomitus; toxicologic analysis of water, vomitus, feces, or liver for nodularin or microcystin
291
what drug should be given with blue-green algae toxicosis and why?
cholestyramine - binds cyanotoxins in gut
292
discuss the mechanism of cycad palm hepatotoxicity
cycasin is bioactivated to methylazoxymethanol by gut bacteria; this metabolite leads to GI and hepatic toxicosis. neurologic signs are seen, too
293
primary hepatic tumors are what % of all tumors in dogs?
0.6-1.5%
294
primary liver tumors are what % of all tumors in cats?
1-3%
295
how much more common are metastatic tumors than primary liver tumors in dogs?
3x
296
are primary or metastatic liver tumors more common in cats?
primary
297
most common liver tumor in dog?
HCC
298
what is the most common primary eline hepatobiliary tumor?
bile duct adenoma
299
which lobes are affected most commonly in HCC?
left lateral and medial and the caudate lobe
300
if a HCC metastasizes, which places are most likely? what is the met rate?
regional LNN, peritoneum, lungs. for massive HCC - 0-37%; for nodular/diffuse - 93-100%
301
what breed & gender are predisposed to canine bile duct tumor?
labrador retriever; female
302
describe biologic behavior of primary hepatic neuroendocrine tumors
aggressive, usually not surgically resectable due to diffuse nature; metastasize to regional LNN, peritoneum, lungs >> heart, spleen, kidney, adrenal glands, pancreas
303
how good is RT for liver tumors?
bad. liver is very sensitive to low radiation, and there's difficulty limiting tissue exposure
304
in general HCC is chemo-resistant. what two drugs have shown to maybe have some effect in dogs?
gemcitabine & mitoxantrone
305
treatment: bile duct carcinoma
none
306
prognostic factors for dogs with massive HCC?
tumor location, serum ALT and AST, ratio of ALP to AST and ALT to AST, histopathologic subtype and anapestic characteristics
307
MST of dogs with massive HCC managed by liver lobectomy versus conservative therapy?
sx: not reached after 1460 days of follow-up. medical: 270d
308
prognosis for cats with surgically resectable bile duct adenoma?
excellent - no reports of local recurrence or malignant transformation
309
what is the path that bile takes to get into the GB?
formed in hepatocytes. actively secreted into bile acnaliculi. then into interlobular ducts and ultimately lobar ducts. lobar ducts give rise to left and right hepatic ducts. cystic duct is offshoot of hepatic ducts and travels towards GB
310
what is bile made of?
cholesterol, lecithin, phospholipids, bile salts
311
what is the purpose of bile?
emulsify fat and neutralize acid in partially digested food
312
what is the difference between dog & cat bile tract anatomy?
dog: CBD joins minor pancreatic duct and both exit separately at major duodenal papillae. cat: CBD fuses with major pancreatic duct before entering the duodenum
313
what signalment is predisposed to choleliths?
old, female dogs. mini schnauzer & mini poodle
314
describe the physiology behind cholelith formation
cholesterol is strongly hydrophobic, necessitating transport in micelles to remain suspended in solution. when an imbalance occurs between bile salts and cholesterol, bile becomes more viscous leading to formation of gallstones.
315
what predisposes a patient to developing choleliths?
gallbladder dyskinesia, hypercholesterolemia, hypertriglyceridemia, hyperbilirubinemia, endocrine disease, cholesterol absorption and transport defects in GB
316
in cats, a CBD diameter greater than X mm is indicative of extra hepatic biliary obstruction
5mm
317
what factors predispose an animal to cholecystitis?
bile stasis, GB mucocele, ascending bacterial or parasitic diseases, biliary neoplasia, infarction, hematogenous spread of bacteria. in cats, bacterial infections are thought to be secondary to inflammation rather than the inciting factor.
318
what characteristic of abdominal effusion allows you to diagnose it as biliary rupture?
bilirubin in effusion is > 2x that in circulating blood
319
in cats, a GB wall thickness of > x mm predicts GB dz
1mm
320
what are the most common isolates in cholecystitis?
E coli, enterococcus, bactericides, streptococcus, clostridium, helicobacter
321
emphysematous cholecystitis has been associated with which diseases?
diabetes mellitus
322
what is the most appropriate treatment for emphysematous cholecystitis?
surgical intervention
323
what bacteria are most commonly isolated in emphysematous cholecystitis?
anaerobes, E coli, clostridium perfringens
324
which antibiotics are best for empirical use in cholecystitis?
fluoroquinolones, metronidazole, chloramphenicol - high concentrations in bile, strong anaerobic activity
325
discuss pathogenicity of biliary cystadenomas
rarely make a problem; may need to be surgically resected if space-occupying problems arise. favorable prognosis
326
name 3 species of flukes that infect feline biliary tract & liver
platynosomum fastosum, platynosomum concinnum, amphimerus pseudofelineus
327
describe the life cycle of hepatobiliary flukes
ova of flukes passed in cat feces. land snail ingests ova. amphibian or reptile (toad, gecko, lizard) eats the snail. cat eats the second intermediate host.
328
are cats always symptomatic for hepatobiliary flukes?
no, some arasymptomatic carriers
329
what is the most reliable method of diagnosing hepatobiliary parasites?
fecal sediment; aspiration & cytology of bile are useful for ID'ing fluke eggs if fecal is negative
330
treatment for biliary flukes?
praziquantel; consider steroids & antihistamines prior to treatment to control inflammatory response. surgery if biliary obstruction. abx if neutrophilic cholangitis on histopath
331
list the predisposing factors for a biliary mucocele
dyslipidemia, dysmotility of GB, endocrine disease, exogenous steroid administration. sheltie, cocker, mini schnauzer. in cats, biliary stasis and congenital biliary abnormalities are thought to play a role.
332
why do steroids cause an increased risk of mucocele?
high dose steroids lead to higher unconjugated bile acids within extra hepatic biliary tree. unconjugated bile acids are more hydrophobic and when in disproportionate levels, lead to injury of biliary epithelium. ucin secretion increases as a result of the injury and ultimately leads to mutinous hyperplasia
333
how does hypothyroidism predispose animals to GB mucocele formation?
reduced bile flow; sphincter of Oddi relaxation impaired, liver cholesterol metabolism altered and bile secretion diminishes. mucin organizes and solidifies under these conditions.
334
shelties treated with this drug are more likely to develop a mucocele
imidacloprid (in flea control products)
335
what liver enzyme is predominantly elevated in GB mucoceles?
ALP
336
what bacterial organisms are most commonly found in patients with mucoceles?
enterococcus, enterobacter, E coli, staph, strep
337
what type of diet should be given to a patient undergoing medical therapy for a mucocele?
low fat
