Liver Pathology Flashcards
1
Q
What does a Normal liver look like?
A
2
Q
What are the major structural components of the liver?
A
- Connective tissue capsule, trabeculae and reticular network forms the framework for hepatic architecture
- Sinusoids and hepatic cords
- Biliary tree
3
Q
What are major cells of the liver?
A
- Hepatocytes
- Kupffer cells
- Stellate cells
- Endothelial cells
- Biliary epithelium
4
Q
What is a hepatic lobule?
A
- An anatomic unit with the central vein at the center of the lobule and portal triads at the periphery
5
Q
What is a hepatic acinus?
A
- A functional unit with the central axis bridging between portal areas (1) with the outer part of the acinus around the central vein (3)
6
Q
Describe hepatocytes
A
- Account for approximately 80% of total liver mass
- Arranged in branching, single-cell plates between sinusoids
- Numerous microvilli on the surface facing the sinusoid
- Contain numerous intracellular organelles
7
Q
What are the functions of hepatocytes?
A
- Responsible for most of the synthetic secretory, storage, detoxification, and metabolic functions of the liver
- Produce and secrete bile into the bile canaliculi
8
Q
Describe Kupffer cells and their functions
A
- Member of the mononuclear phagocyte system
- Mobile macrophages located within the sinusoids
- Phagocytose immune complexes and particulate matter (senescent RBC, bacteria, etc) in the sinusoids
- Produce pro-inflammatory and anti-inflammatory cytokines to contribute to innate immunity
- Pro-inflammatory products (TNF-alpha) can activate hepatic stellate cells to create collagen
9
Q
What are the hepatic stellate (Ito) cells
A
- Located in the Space of Disse
- Store Vit A
- During hepatic injury:
- convert to a myofibroblast phenotype and produce collagen and other ECM components to promote hepatic fibrosis
10
Q
What is Sinusoidal Endothelium?
A
- Second most common cell in the liver
- 15-20% of all cells, only 3% of liver mass
- Contain numerous fenestrae
- They lack a well organized basement membrane
- Discontinuous capillary allows intimate contact with blood components and hepatocytes
- Facilitate exchanges between plasma and hepatocytes
11
Q
How is blood supplied to the liver?
A
- Liver has a dual blood supply
- Hepatic artery (O2)
- Portal vein (high nutrient blood)
- Blood flow is from the portal triad to the central vein
- Discontinuous capillary with fenestrated endothelium allows intimate contact with blood components and hepatocytes
12
Q
How does the liver produce lymph?
A
- Fluid from the hepatic interstitium flows into the space of Disse then to the portal interstitium to the portal lymphatics
- The fluid is derived from the blood as well as products of hepatocytes, hepatic stellate cells and Kupffer cells
- The liver accounts for 50% of lymph that enters the thoracic duct
- The role of lymphatics in disease is poorly understood
- obesity, lipidosis, hypercholesterolemia, lipoprotein-associated diseases
13
Q
What is the pathway of bile from the hepatocytes?
A
- Bile is transported from the hepatocyte through a progressively enlarging duct system for secretion into the small intestine
- Bile canaliculi
- Intrahepatic bile ductules (Canals of Hering)
- Intralobular bile ducts (portal triads)
- Intralobular ducts (joint into intralobar ducts then lobar)
- Lobar ducts
- Extrahepatic (common) bile duct
14
Q
What is Bile made up of?
A
- Water
- Bile salts
- Bilirubin
- Cholesterol
- Fatty acids
- Lecithin
15
Q
How many liver lobes do the different species have?
A
- Dogs/Cats 6
- Left lateral, left medial, quadrate, right medial, right lateral, caudate
- Mice/Rats 4
- Left, middle, right, caudate
- Horse 5
- right, quadrate, left medial, left lateral, caudate
- Bovine and humans 4
- right, caudate, left, quadrate
- Elephant and avian 2
- left, right
- Pigs 5
- left medial, left lateral, right medial, right lateral, caudate
16
Q
What species do NOT have a gallbladder?
A
- Equines - horses, mules, etc
- Cervids - white-tailed deer….
- exception is musk deer
- Camels
- Rats
- Elephants
- Giraffes
- often present in neonates
- Rhinoceroses
- Doves, pigeons, ostriches, and some psittacines
- most avian species have gall bladders
- others
17
Q
What is the function of the Liver?
A
- Plays a central role in metabolism
- Synthesis and metabolism of proteins, lipids, and carbohydrates
- Storage of nutrients
- Conjugation and detoxification reactions
- Immune functions
- Waste product excretion
- Bile synthesis of secretion
18
Q
What nutrient synthesis, storage, and metabolism functions does the liver have?
A
- Glucose metabolism
- Degradation of plasma lipids and synthesis/storage/oxidation of fatty acids
- Production of most plasma proteins
- Production of cholesterol and lipoproteins
- Nutrient storage
- Glycogen and lipids
19
Q
What are the conjugation and detoxification functions of the Liver?
A
- Xenobiotic biotransformation and excretion
- Phase I reactions
- Convert toxins into less (sometimes more) harmful intermediate compounds
- Cytochrome P-450 enzymes
- Convert toxins into less (sometimes more) harmful intermediate compounds
- Phase II reactions
- Convert Phase I products into water soluble products for excretion
- Conjugation reactions (glucuronidation, sulfation, gluthathione, and AA conjugations)
- Convert Phase I products into water soluble products for excretion
20
Q
What are the immune functions of the liver?
A
- Remove foreign material from blood
- Kupffer cells
- Hepatocyte protein synthesis
- Inflammation (acute phase proteins) and innate immunity and signaling pathways
21
Q
How is Bile synthesized in the liver?
A
- Bilirubin is derived from hemoglobin and other heme proteins
- Bilirubin is taken up by hepatocytes, conjugated to glucuronic acid to become water soluble and less toxic and excreted through the biliary system
- Bile acids are produced by hepatocytes and efficiently recycled by the enterohepatic circulation
- Bile acids are essential for digestion and absorption of lipids and fat-soluble vitamins
- Excretion of waste products and metabolites
22
Q
How is liver dysfunction determined?
A
- The liver has alarge functional reserve capacity
- Clinical evidence of disease may initially be absent
- There are a wide variety of clinical assays to use to evaluate liver function
- Liver enzymes:
- Gamma-glutamyl transpeptidase (GGT)
- Alkaline phosphatase (ALP)
- Alanine transminase (ALT)
- Aspartate transaminase (AST)
- Bilirubin, bile products, albumin, total protein
- Prothrombin time
- Liver enzymes:
23
Q
What are the clinical signs of hepatic disease?
A
- Icterus
- Photosensitization
- Encephalopathy
- Hemorrhage
- Edema
- GI distrubances
- Untrhiftiness
24
Q
What is Icterus?
A
- Excess bilirubin (hyperbilirubinemia) results in yellow discoloration of tissue
- Causes:
- Overproduction
- hemolysis or excessive RBC degradation
- Hepatocyte injury
- decreased uptake, conjugation, or secretion of bilirubin
- Decreased bile flow (cholestais)
- Intrahepatic (bile canaliculi)
- Extrahepatic (bile ducts/gall bladder
- Overproduction
25
What is photosensitization?
* Activation of pigments by UV light causes erythema, hair loss, and dermal necrosis
* **Type** 1 - increased ingestion of photodynamic pigments
* **Type 2** - abnormal metabolism of photodynamic pigments
* **Type 3** - decreased secretion of photodynamic pigments
26
How does liver disease lead to encephalopathy?
* Accumulation of ammonia, toxic products and neurotransmitter-like substances cause neurologic dysfunction
* These substances are normally excreted by the liver
* Accumulation can be due to decreased metabolism by the liver or vascular shunting past the liver
* Signs ranged from depression to convulsions
27
How does liver disease lead to hemorrhage?
* All clotting factors are produced by the liver
* Factor VIII is on e possible exception
* With severe hepatic injury, decreased production can result in defective secondary hemostasis
28
How does liver disease lead to edema?
* Albumin, produced mainly by the liver, regulates plasma osmotic pressure
* Hypoalbuminemia results in fluid imbalance and edema
29
How does liver disease cause GI distrubances?
* Decreased bile secretion will disrupt digestion
* Decreased bile acids decrease fat and fat-soluble vitamin absorption
30
How does liver disease result in unthriftiness?
* Chronic liver dysfunction results in weight loss and poor conditions
* Hypoalbuminemia
* Altered fat and protein metabolism
* Altered digestion
31
What are examples of acute hepatic disease?
* Icterus
* GI abnormalities
32
What are examples of chronic hepatic disease?
* Weight loss
* Unthriftines
33
What are the Pathological Processes that affect the liver?
* Cell adaptation and injury
* Tissue injury
* Vascular disturbances
* Inflammation
* Immunopathology
* Developmental
* Metabolic
* Neoplasia
34
What is Regenerative hyperplasia?
* Hepatocytes can rapidly transition for G0 to G1
* Localized or a single episode of extensive damage can return to normal morphology by compensatory hyperplasia if the structural framework is intact
* If the structural framework is damaged: hyperplasia occurs in a nodular morphology (regenerative nodules)
* usually in combination with hepatic fibrosis
35
What is hepatocyte Nodular hyperplasia?
* Most common in older dogs
* Rarely associated with _hepatic dysfunction_
* Normal hepatic framework is infringed upon by hyperplastic hepatocytes
* There is **no fibrosis** associated with the nodules
* Hyperplastic nodules have **reduced function**
* Blood and bile flow within nodules is **abnormal**
36
What is hepatocyte cirrhosis?
* **Regenerative hyperplasia + fibrosis**
* “End-stage liver”
* An **irreversible**, final outcome of a variety of progressive hepatic diseases (toxicity, chronic inflammation, biliary disease)
* Morphology is severely distorted
* Associated with signs of hepatic failure
37
What is cholangiolar hyperplasia ("ductular reaction")
* Hyperplasia of progenitor cell around the portal triads than can differentiate into either hepatocytes of bile duct epithelium
* A non-specific response to various diseases, including toxicity, cholestasis, and hypoxia
* Morphologically these form multiple duct-like structures in the portal area
38
What is hepatocyte atrophy?
* Most common in hepatocytes that **have lost normal vascular and nutrient supply**
* Acquired portosystemic shunts due to hepatic fibrosis
* Starvation after all body nutrient stores are depleted
* **Hepatocytes are smaller and may be reduced in number**
* The liver is smaller than normal
* Remember that a small liver in a neonatal animal is most likely a developmental problem7
* Hypoplasia
39
What are the common causes of hepatocyte injury?
* **Chemicals**
* Xenobiotics (toxins), endogenous and exogenous substances
* **Nutrients**
* Too few (hypoxia)
* Too many (lipidosis)
* **Infectious agents**
* Bacterial
* Viral
* Fungal
40
What are the Mechanisms for Hepatocyte injury?
* **Loss of membrane integrity**
* Cell membranes breakdown and loose the ability to segregate reactions within the cell
* Free radicals
* Phospholipases
* Direct membrane injury
* **Loss of ability to produce energy**
* ATP is insufficient to support cell functions
* Oxidative phosphorylation and glycolysis
* **Genetic damage**
* functional changes induced by a mutation
41
What are the morphologic features of injured hepatocytes?
* Sublethal Injury: (potentially reversible)
* Cell swelling
* Intracellular accumulations
* Neoplastic transformation
* Lethal injury:
* Apoptosis
* Necrosis (oncotic death)
42
What is happening in the image?
cell swelling
43
What is happening in the image?
lipidosis
44
What is happening in the image?
* Cell swelling _and_ lipidosis
* Often concurrent - reflecting a gradient of injury
45
What causes sublethal hepatocyte injury?
* Hepatotoxins
* Hypoxia
46
What causes Lipidosis?
* Lipidosis can also be a physiologic change unrelated to hepatocyte injury:
* High fat ration
* Increased periparturient energy needs
* Anorexia
47
What are the **lethal** hepatocyte injuries?
* Apoptosis
* Necrosis
48
What are the causes of hepatocyte Apoptosis?
* Physiologic:
* **maintenance of homeostasis**
* Pathologic:
* **Unrepaired DNA damage**
* damaged or transformed cells
* **Heat**
* **Hypoxia**
* Mitochondrial injury
* **Viral infection**
* **Physical pressure**
49
What are the causes of hepatocyte necrosis?
* Unintentional and passive
* Caused by _pathologic injury_ to the hepatocyte
* Hypoxia
* Toxins
* Infectious agents
* Many of the same factors that initiate apoptosis when the stimulus is mild, initiate necrosis when more severe
* Hepatocyte undergoes passive self-lysis
50
What are the morphologic patterns of necrosis of injury?
* **Zonal** (lobular)
* There is a _repeating pattern_ of necrosis within the hepatic lobule - commonly due to toxins or hypoxia
* Common:
* **Centrilobular**
* **Periportal**
* Less Common:
* **Paracentral-** wedge-shaped area radiating out from the center
* **Midzonal** - Midway between portal and central
* **Massive** - An entire lobule is affected
* **Multifocal:**
* Hepatocytes are affected randomly
* Commonly due to blood-borne infectious agents
51
What is the centrilobular (periacinar) pattern of hepatic necrosis?
* Centrilobular hepatocytes are mainly affected
* Causes:
* Hypoxia
* Nutrient deficiency
* Toxins that are biotransformed into toxic intermediate compounds
52
What is the periportal (Centriacinar) pattern of hepatic necrosis?
* Periportal hepatocytes are mainly affected
* Causes:
* **Ascending biliary infections**
* **Toxins (direct-acting)**
53
What is the multifocal pattern of hepatic necrosis?
* Hepatocytes are affected randomly
* Causes:
* Blood-borne infectious agents
* Viruses often causes hepatic necrosis with variable amounts of inflammation
* Certain bacteria produce toxic substances or invade hepatocytes and can result in extensive necrosis
54
What are some causes of hepatic necrosis?
(Not viral or bacterial)
* **Plant toxins**
* Pyrrolizidine alkaloids
* Glycosides
* **Mycotoxins**
* Aflatoxins
* Sporidesmin
* Phomosins
* **Cyanobacteria**
* **Chemicals**
* Phosphorus
* Carbon tetrachloride
* Cresols
* **Drugs**
* Acetaminophen
* Carprofen
* Anticonvulsants (phenobarbital)
* Tranquilizers (diazepam)
* **Metals**
* Iron
* Copper (ruminants)
* **Nutrients/Food additives**
* Vitamin E/Selenium deficiency
* Hypoxia
* Xylitol
55
What are some of the viral and bacterial causes of hepatic necrosis?
* Viruses:
* Herpesvirus
* Dog, cat, bovine, horse, pig
* Rif Valley Fever/ Wesselbron disease
* Canine adenovirus-1
* Infectious canine hepatitis
* Hepadnavirus
* Woodchuck hepatitis virus
* Bacteria:
* *Clostridium haemolyticum*
* Bacillary hemoglobinuria
* *Clostridium novyi*
* Infectious necrotic hepatitis
* *Clostridium piliformis*
* Tyzzers disease
* *Fusobacterium necrophorum*
* Hepatic “abscesses”
* *Trueperella pyogenes*
* “real” hepatic abscesses
56
What causes Extracellular matrix injury?
* A reflection of damage to both cells and extracellular matrix
* Causes:
* **Fibrosis**
* **Amyloidosis**
* **Calcification**
57
What is hepatic fibrosis?
* Fibrosis is a common manifestation of hepatic injury
* Causes of fibrosis include almost any (mainly recurring) insult:
* Cell injury
* Vascular disturbances
* Inflammation
* Mediation of fibrosis
* Hepatic stellate cells
* Located in the Space of Disse
* Myofibroblasts
* Located in connective tissue of portal areas and central veins
58
What are the possible morphologies of hepatic fibrosis?
* **Periportal** - direct-acting toxins or biliary inflammation
* **Centrilobular** - Indirect-acting (biotransformed) toxins or hypoxia
* **Bridging (Diffuse)** - Progressive, ongoing fibrosis
* Fibrosis can significantly alter the ECM and hepatic architecture
59
What is hepatic cirrhosis?
* Sometimes referred to as “end-stage liver”
* Morphologically these are characterized by fibrosis and regenerative hyperplastic nodules
* This is characteristic of severe chronic and progressive hepatic injury
60
What are the vascular disturbances that affect the liver?
* Passive congestion - common
* usually secondary to heart failure
* Vascular shunts - less common
* Congenital shunts are a developmental abnormality of vessel formation
* Acquired shunts are usually secondary to vascular obstruction due to fibrosis
61
How does chronic passive congestion affect the heart?
* Right heart failure
* Initially there is centrilobular congestion
* Progressive hypoxia leads to centrilobular hepatocyte necrosis
* Chronically, there is centrilobular fibrosis and periportal pooling of blood
* Ascites can occur due to portal hypertension
* “nutmeg liver”
62
How doe acquired vascular (portosystemic) shunts affect the liver?
* **Disruption of hepatic bloo**d flow due to a portal hypertension, usually secondary to hepatic fibrosis, vascular damage or inflammation.
* These may be **asymptomatic**, or result in **encephalopathy**, **ascites**, or other signs of hepatic disease
* **Congenital shunts** can also occur due to developmental anomalies of hepatic vessels resulting in shunting of blood past the liver
63
What is liver inflammation?
* A wide variety of infectious agents and non-infectious reactions can induce inflammation
* Viruses, bacteria, fungi, parasites, immunologic responses
* The morphology of the inflammation often suggests cause
* Suppurative = bacterial
* Lymphocytic = viral
* Granulomatous = fungal or higher bacteria
64
What are the categories of liver inflammation?
* Hepatitis (Acute & Chronic)
* Cholangitis
* Cholangiohepatitis
65
What are immunologic injury causes of hepatic/biliary inflammation?
* Idiopathic ("Autoimmune") Chronic hepatitis in dogs
* Immune mediated feline cholangitis/cholangiohepatitis
66
What fungi can cause hepatic/biliary inflammation?
* *Histoplasma capsulatum*
67
What viruses can cause hepatic/biliary inflammation?
* Feline coronavirus
* Feline infectious peritonitis
* Canine adenovirus - 1
* Herpesvirus
68
What bacteria can cause hepatic/biliary inflammation?
* Enteric bacteria
* *E. coli*
* *Enterococci*
* Among others
* *Salmonella sp.*
* *Mycobacterium sp.*
* *Corynebacterium pseudotuberculosis*
* *Francisella tularensis*
* *Clostridium piliformis*
* Tyzzers disease
* *Trueperella pyogenes*
* “real” hepatic abscesses
69
What immune mediate reactions of the liver are inadequately characterized?
* Idiopathic ("autoimmune") chronic hepatitis in dogs
* Immune mediated feline cholangitis/cholangiohepatitis
* Idiopathic acute hepatic disease of horses (Theiler disease)
70
What are some Developmental anomalies of the Liver?
* Hepatic cysts
* Hepatic hypoplasia
* Congenital portosystemic shunts
71
What are hepatic cysts?
* Often biliary origin
* In cats these often occur as part of polycycstic kidney disease
* Defective polycystin due to PKD-1 or PKD-2 gene mutations
* Most common in Persian cats
* Progressive renal disease
72
What is hepatic hypoplasia?
* Most commonly due to vascular maldevelopment in the liver
* Microvascular dysplasia
* Congenital portosystemic shunts
73
What is Microvascular dysplasia?
* Most prevalent in small breed dogs (Yorkshire and Cairn Terriers among others)
* Abnormal development of branches of the portal vein, with compensatory increase in hepatic arteries that take on a coiled appearance
* Clinical features/lesion are similar lesions to congenital portosystemic shunts
74
What are congenital Portosystemic shunts?
* Congenital shunts are due to vascular abnormalities that shunt blood past the liver
* Microvascular dysplasia is one component of portosystemic shunts
* Intra- or extra-hepatic vascular abnormalities are present
* Affects livers lack adequate nutrients and are hypoplastic and have inadequate functions
75
What metabolic disturbances can occur with hepatic diseases?
* Alteration in hepatic metabolic function accompany most primary hepatic diseases and many secondary non-hepatic disease
* **Altered plasma protein production can influence various homeostatic processes**
* _Albumin_ - fluid balance and edema
* _Coagulation factors_ - hemorrhage and hemostasis
* _Acute phase proteins_ - inflammation
* **Bilirubin metabolism and bile flow influence digestion**
* Bilirubin accumulates when there is excessive production (eg hemolysis) decreased hepatocyte function, or decreased biliary flow (cholestasis)
* Cholestasis can be intrahepatic (ex: hepatocyte injury or hemolysis) or extrahepatic (extrahepatic bile duct obstruction)
* Decreased bile acids results in lipid malabsorption/steatorrhea and deficiency of fat-soluble vitamins
76
What is hepatic lipidosis?
* Liver is central to fat metabolism and involves proteins, fats, carbohydrates, and energy
* **Metabolic imbalance can result in lipidosis**
* Increased rate of fat entry to hepatocytes
* Decreased rate of lipoprotein formation within hepatocytes
* Decreased protein or energy (ATP)
* Increased carbohydrates
* Some degree of lipidosis accompanies many metabolic alterations
77
What are some metabolic alterations result in lipidosis?
* Toxicity
* Hypoxia
* Endocrine disorders
* Nutritional problems
* Physiological changes
* Periparturient events
78
What are some specific lipidosis syndromes?
* Feline fatty liver syndrome
* Bovine fatty liver syndrome/ketosis
* Hyperlipidemia of ponies
79
What is going on with this cat?
feline fatty liver syndrome
80
What is glycogenosis?
* Any abnormality of glucose will alter glycogen stored in the hepatocytes
* Glycogen is the storage from of glucose
81
What are common conditions associated with glycogen accumulation?
* Diabetes mellitus
* Hyperadrenocorticism
* “steroid hepatopathy”
* Benign vacuolar hepatopathy
82
What is the morphology of glycogenosis?
* Morphologically, hepatocytes have a swollen, foamy appearance
* Due to excessive glycogen in the cytoplasm
* Distribution tends to be diffuse
* Cell swelling is a differential
* This is usually more localized or zonal
83
What are the Mechanisms of Action of Hepatotoxicity?
* Direct injury to hepatocytes
* Membrane damage, or damage to membrane pumps
* Formation of toxic intermediate products
* The most common mechanism of injury
* Chemical agent is not toxic until biotransformed
* Lipid peroxidation
* Mitochondrial or plasma membranes
* Interference with metabolism
84
What are the functional effects of Hepatotoxicity?
* Decreased protein and nucleic acid synthesis
* Enzyme inhibition
* Inhibition of mitosis
* Cell membrane dysfunction
* Carcinogenesis
* Idiosyncratic reactions
85
What are the different morphologies of hepatotoxicity?
* Hepatocyte injury
* Fibrosis
* Inflammation
* Hyperplasia is common in chronic toxicities
* Changes in cell size
86
What is the Morphology of hepatocyte injury due to Hepatotoxicity?
* Degeneration
* Hydropic change
* Lipidosis
* Necrosis or apoptosis
* Centrilobular necrosis is most common due to indirect acting toxins
* Periportal necrosis occurs with direct acting toxins
87
What is the morphology of fibrosis caused by hepatotoxicity?
* Most common with recurrent injury
* Results in irreversible stromal damage
* It is a c**ommon feature of most hepatotoxins** over time
88
How does inflammation result from hepatotoxicity?
* Can occur in response to necrotic cells which result from toxin exposure
* Binding of toxins to cell products may alter the products so they are regarded as foreign
* Idiosyncratic reaction
* Hepatoallergens
* Immune-mediated inflammation
89
How does hyperplasia result from hepatotoxicity?
* Hyperplasia is common in chronic toxicities
* Nodular regeneration
* Cholangiolar hypergplasia (biliary epithelial hyperplasia)
* Located around portal triads
90
How do changes in cell sizes result from hepatotoxicity?
* Megalocytosis
* occurs due to toxin-induced inhibition of mitosis
* Most common with pyrrolizidine alkaloid and aflatoxin toxicity
91
What are the clinical manifestations of **acute** hepatotoxicity?
* Acute death
* Icterus
* GI problems
92
What are the clinical manifestations of chronic hepatotoxicity?
* Unthriftiness and weight loss
* Multiple metabolic disturbances
93
What are some causes of hepatotoxicity?
* Bacterial/fungal products
* **Aflatoxins**
* Plant products
* **Pyrrolizidine alkaloids**
* Pharmacological agents
* **Carprofen**
* Chemicals
* **White phosphorus**
94
What causes Liver neoplasia?
* Due to mutation and cell transformations
* Causes:
* Inherited
* Chemical exposure
* Alfatoxins and pyrrolizidine alkaloids
* Infectious agents
* Woodchuck hepatitis virus (model for Hepatitis B virus in humans)
* FeLV, BLV (lymphosarcoma - metastatic)
95
What genes are commonly affected to cause liver neoplasia?
* Genes that promote cell growth and division
* Protooncogenes
* Genes that inhibit cell growth and division
* Tumor suppressor genes
* Genes that regulate DNA repair
* Genes that regulate apoptosis
96
What are some primary liver neoplasias?
* Hepatocellular adenoma/carcinoma
* Arise from hepatocytes
* Cholangiocellular adenoma/carcinoma
* arise from biliary epithelium
* Mesenchymal cells within the liver
* Hemangiosarcoma, fibrosarcoma
97
What are some metastatic liver neoplasias?
* Hemangiosarcoma
* Lymphosarcoma
* Mammary carcinoma
98
What is Hepatic adenoma?
* Benign neoplasm of hepatocytes
* Most common in young ruminants and old dogs
* Must be differentiated from nodular hyperplasia
99
What is hepatocellular carcinoma?
* Most common primary hepatic neoplasm in dogs
* Locally invasive within the liver
* Some will metastasize to regional lymph nodes
100
What is a Bile duct adenoma?
* Biliary cystadenomas
* Benign and cystic
* Most common primary hepatic neoplasm of cats
* Account for about half of primary tumors in cat livers
101
What is a bile duct carcinoma?
* Cholangiocellular carcinoma
* Most common primary malignant liver neoplasm of cats
* Less common than hepatocellular carcinoma in dogs
* Metastasis is common to regional lymph nodes and by seeding of the peritoneal cavity
102
What is going on in the picture?
Intestinal adenocarcinoma
103
What is going on in this picture?
Hemangiosarcoma
