Unit 4 - Liver 1 Flashcards
1
Q
What are some of the major liver functions?
A
protein metabolism, carbohydrate and lipid metabolism, detoxification, hormone and vitamin metabolism, storage, digestive, hematologic, and immunologic functions
2
Q
What proteins does the liver create?
A
albumin, carrier proteins, clotting, factors, and many acute phase proteins
3
Q
How does the liver produce urea?
A
via protein catabolism causing deamination of amino acids leading to urea
4
Q
What does the liver metabolize?
A
glycogen, ketones, cholesterol
5
Q
How does the liver create bilirubin?
A
by catabolising heme
6
Q
What are some clinical signs of hepatic disease?
A
icterus, hepatic encephalopathy, photosensitization, ascites, and hemorrhage
7
Q
What can cause hepatic encephalopathy?
A
hypoglycemia, increased blood ammonia, increased GABA, toxic amines, aromatic Aas
8
Q
How can hepatic disease lead to photosensitization?
A
Phylloerythrin is ineffectively removed by the diseased liver and accumulates in the skin
9
Q
What are the liver causes of ascites?
A
portal hypertension or hypoalbuminemia
10
Q
How does hepatic disease cause hemorrhage?
A
decreased production of clotting factors or massive necrosis initiating the clotting cascade
11
Q
What is icterus/jaundice?
A
yellowish discoloration of tissues caused by hyperbilirubinemia
12
Q
True or False: Icterus is specific for liver disease
A
FALSE
13
Q
What are the general hepatic causes of icterus/jaundice?
A
pre-hepatic, hepatic, and post-hepatic
14
Q
What is an example of a pre-hepatic cause of icterus/jaundice?
A
overproduction - ie hemolysis
15
Q
What can cause hepatic icterus/jaundice?
A
impaired uptake, metabolism, secretion, and/or transport of bile in the liver OR can be due to hepatocellular degeneration, swelling, or necrosis
16
Q
What can cause post-hepatic icterus/jaundice?
A
biliary duct obstruction typically due to intra-luminal or extra-luminal masses/inflammation
17
Q
If the liver is not functional what will the bile acids be like in serum?
A
they will be elevated
18
Q
What are considered the leakage enzymes?
A
ALT, AST, and SDH
19
Q
What is considered the hepatic induced secreted enzymes?
A
ALP
20
Q
With liver disease, what may the level of bilirubin look like on serum biochemistries?
A
it may be elevated
21
Q
In hepatic disease, what will the level of serum bile look like?
A
it will be elevated
22
Q
What will the levels of BUN and albumin be like in cases of liver disease?
A
it may be decreased since they are produced by the liver
23
Q
What are some clinical ways to evaluate hepatic disease grossly?
A
radiography, ultrasoumd, contrast studies, or visualize during laparotomy/laparoscopy
24
Q
What is a common hepatic lesion seen in older dogs?
A
nodular hyperplasia
25
What are some ways to biopsy a liver (cuts)?
wedge or percutaneous core
26
What is the general structure of the liver?
hepatocytes, portal tracts, sinusoids, terminal hepatic venules, bile duct, gall bladder
27
What are the componenets of the portal triad?
hepatic artery, portal vein, bile ductule, and lymphatics
28
What are the three liver zones?
periportal zone (zone 1), Midzonal zone (zone 2), and Centrilobular zone (zone 3)
29
What proportion of cardiac output does the liver receive?
1/4 of total cardiac output
30
Of the cardiac output that goes to the liver, what percentage of that is delivered via the portal vein?
75% (low O2)
31
What does the portal vein drain blood from?
the abdominal organs
32
What is the livers role in filtering blood?
it metabolizes absorbed nutrients and removes absorbed tocins
33
What is the remaining 25% of the blood that goes to the liver delivered by?
the hepatic artery (high O2)
34
What does reduced hepatic blood flow lead to? Increased blood flow?
atrophy, hypertrophy
35
What are some selected diseases of liver vasculature?
passive congestion, portosystemic shunts
36
What is the cause of passive congestion in the hepatic vasculature?
increased pressure in the hepatic veins
37
What is passive congestion typically due to?
right sided heart failure
38
What is the appearance of acute hepatic passive congestion?
the liver is enlarged and dark in color (congested)
39
What is an example of acute hepatic passive congestion?
Mullberry Heart Disease in swine
40
What is chronic hepatic passive congestion also known as?
nutmeg liver
41
What is the appearance of chronic hepatic passive congestion?
the liver is speckled, dark red areas represent dilated and congested central sinusoids and venules, the pale areas are intact periportal region with fatty change
42
What is chronic hepatic passive congestion often accompanied by?
ascites
43
What microscopic lesions are associated with hepatic passive congestion?
degeneration/necrosis of centrilobular hepatocytes, central veins, hepatic veins, and sinusoids are dilated
44
What is a portosystemic shunt?
an abnormal communication between the portal vein and systemic circulation, bypassing the liver
45
What are some results of a portosystemic shunt?
reduced hepatic circulation leading to microhepatica (small liver) and bacteria, toxins, and ammonia are not removed by the liver and enter the circulation
46
What is the most common cause of hepatic encephalopathy in young dogs and cats?
portosystemic shunts
47
When do clinical signs from congenital portosystemic shunts show up?
at 6-18 months of age
48
What clinical signs are associated with congeintal portosystemic shunts?
small body size, vomitting and/or diarrhea, polyuria/poydyspsia, anesthetic intolerance, and behavioral abnormalities
49
What behavioral abnormalities are associated with congenital portosystemic shunts?
ataxia, seizures, blindness, and head pressing
50
When are clinical signs due to congenital portosystemic shunts more noticeable?
after eating
51
What is the severity of clinical signs due to a congenital portosystemic shunt dependent on?
the size of the shunt
52
What are the types of congenital portosystemic shunts?
intrahepatic, extrahepatic, and hepatic microvascular dysplasia
53
When do clinical signs from congenital intrahepatic shunts show?
6-18 months
54
What breeds/species is congenital intrahepatic shunts observed in?
large and giant breed dogs and cats
55
What are the types of congenital intrahepatic shunts?
failure of ductus venosus to close at birth or arise from 1 of the 3 main branches of the portal vein and enter the caudal vena cava directly or via a large branch of the hepatic vein
56
What breeds/species are congenital extrahepatic shunts observed in?
young small and toy breeds (signs 6-18 months) and cats
57
What do extrahepatic shunts arise from?
the main trunk of the portal vein or one of its major tributaries and typically empty into the caudal vena cava or azygos vein
58
What is a portocaval shunt?
a shunt between the portal vein and vena cava
59
What is a portoazygos shunt?
a shunt between the portal vein and azygos vein
60
What is hepatic microvascular dysplasia?
when the microvasculature of the liver is abnormally formed impairing blood flow through the liver
61
What clinical signs are observed with hepatic microvascular dysplasia?
clinical signs similar to those seen with portosystemic shunts
62
What is the average age of presentation of hepatic microvascular dysplasia?
3 years of age
63
What breeds are most commonly affected with hepatic microvascular dysplasia?
small and toy breeds
64
What is liver failure?
the inability to adequately perform normal functions due to insufficient functional hepatic mass
65
What is acute liver failure?
abrupt loss of hepatic function
66
What are some potential causes of acute liver failure?
acute toxic hepatitis or acute infectious hepatitis
67
What can cause acute toxic hepatitis?
poisonous mushrooms or blue-green algae
68
What can cause acute infectious hepatitis?
canine adenovirus 1, Tyzzer's disease, or Leptospira
69
What is chronic liver failure?
progressive loss of hepatic function
70
What lesions are associated with chronic liver failure?
chronic inflammation, fibrosis, nodular regeneration, bile ductule proliferation, acquired vascular shunts
71
What can cause hepatocellular degeneration?
vacuolar change, necrosis and apoptosis, inflammation, fibrosis, hepatocellular regeneration, bile ductule proliferation, and neoplasia
72
What are the three types of vacuolar change?
hydropic change, glycogenn accumulation, and lipidosis
73
What is vacuolar degeneration?
injured hepatocytes that respond by swelling and become vacuolated
74
What may vacuoles distending the cytoplasm contain?
lipid, glycogen, intracellular water (edema), other metabolic wastes or intermediates
75
Is vacuolar degeneration reversible?
generally yes
76
What are some synonyms to hydropic degeneration?
cellular edema or vacuolar degeneration
77
Is hydropic degeneration reversible?
yes
78
What can cause hydropic degeneration?
ischemia, toxins, and metabolic disease
79
What is the pathogenesis of hydropic degeneration?
there is an accumulation of water in the mitochondria and cytocavitary network due to an inability of cells to maintain ionic and fluid homeostasis
80
What gross changes are seen with hydropic degeneration?
the liver is slightly enlarged and pale tan in color
81
What microscopic changes are associated with hydropic degeneration?
the hepatocytes are swollen and have clear to flocculent, eosinophilic cytoplasm
82
What does flocculent mean?
resembling tufts of wool
83
What species does glycogen accumulation occur most commonly in?
dogs
84
What can glycogen accumulation in the liver result from?
glucocorticoids, diabetes mellitus, or glycogen storage diseases
85
What is glycogen accumulation in the liver most commonly due to?
elevated endogenous or exogenous glucocorticoids (steroid hepatopathy)
86
What microscopic changes are associated with glycogen accumulation in the liver?
hepatocelluar vacuolation due to glycogen accumulation
87
Dogs with increased ALP and evidence of vacuolar hepatopathy should be investigated for __________.
hyperadrenocorticism
88
What is another term for hepatic lipidosis?
fatty liver
89
What is hepatic lipidosis?
intracytoplasmic accumulation of triglyceride within hepatocytes
90
When does hepatic lipidosis occur?
when the rate of intrahepatic triglyceride accumulation exceeds degradation and/or release as lipoproteins
91
What are the primary causes of hepatic lipidosis?
excessive delivery of fatty acids to liver, decreased oxidation of fatty acids due to mitochondrialinjury, or impaired lipoprotein synthesis and release
92
What can cause mitochondrial injury leading to decreased oxidation of fatty acids?
toxins and hypoxia
93
What can cause impaired lipoprotein synthesis and release?
toxicity and protein-calorie malnurition
94
What gross changes are associated with hepatic lipidosis?
Liver is enlarged, pale, tan to yellow in color, friable, greasy on cut surface, has rounded edges, may float in formulin and may be icteric
95
What is the microscopic appearance seen in hepatic lipidosis?
multiple small or a few large clear, well-defined vacuoles within hepatocytes, large vacuoles compress the nucleus to the perifery of the cell
96
An obese cat with a history of stress leading to prolonged anorexia shows up on your necropsy table. The cat has hepatic lipidosis. What is the pathogenesis of this lesion?
the anorexia leads to fat mobilization to the liver thus there is a slow rate of triglyceride exported as lipoprotein which causes the fatty liver
97
What is a common liver disease that sheep get during pregnancy?
pregnancy toxemia
98
What clinical signs are associated with pregnancy toxemia?
depression, lethargy, head droop and grinding teath, loss of appetite, and swollen distal limbs
99
You take a urine sample from an ovine suffering from pregnancy toxemia. What do you expect the urine dipstick to show?
it is positive for ketones which are produced by liver from fatty acids during times of negative calorie balance
100
At necropsy, what will the liver look like from an animal suffering from preganncy toxemia?
the liver is enlarged, pale, tan to yellow in color, friable, greasy on cut surfacem has rounded edges, and floats in formalin
101
What can cause pregnancy toxemia?
inadequate caloric intake, increased caloric demand, source of lipid
102
What is the difference microscopically between steroid hepatopathy and hepatic lipidosis?
steroid hepatopathy - clear to flocculent eosinophilic cytoplasm with a central nucleus
Hepatic lipidosis - well-demarcated clear vacuoles. Nucleus frequently compressed to the periphery of the cell
103
What are the routes by which the liver can become infected?
via the bloodstream, ascending infection via the biliary tree, seeded from adjacent structures/tissues, or parasite infection/migration/encystment
104
How can the liver become infected via the bloodstream?
systemic infection or infected via the portal circulation
105
What ascending infection up the biliary tree can infect the liver?
suppurative cholangiohepatitis
106
What pattern do you expect to see in the liver when there is a systemic infection?
small, multifocal, random liver lesions - lesions in other tissues are anticipated
