Exam 3 Flashcards
Hepatobiliary System
Biography of the liver
Largest internal organ in the body
-Adult Carnivores 3-4% og BW
-Adult omnivores, small ruminants 1.5-2% of BW
-Large herbivores 1%
-Location: central cranial abdomen (monogastrics). Ruminants: displaced to the right by the rumen
-The coronary ligament attaches the liver to the diaphragm near the esophagus and the falciform ligament attaches the midline of the liver to the ventral midline of the abdomen.
-Lobation: varies among species
-Domestic animals have 5-6 lobes and each lobes has hepatic lobules approx 700K in the liver. 0.5-2mm in diameter.
-The liver has a smooth capsular surface, parenchyma consists of friable red-brown tissue that is dived into lobes, at the periphery the lobes taper into a sharp edge.
Nutritional blood supply
-Hepatic artery 20-30% blood flow
Functional supply
-Portal vein: 70-80% blood flow
High source of microbe/toxin exposure
Describe the portals of entry into the liver and the defense mechanisms the liver has to minimize disease introductionIdentify the anatomy of the liver.
Describe how the gross and microscopic anatomy play a part into the development of diseases and pattern distribution
The liver and biliary systems are exposed to infectious or otherwise injurious substances via three main routes:
- Hematogenous (viral, bacterial, fungal, etc.)
Localization within sinusoids via
-Portal vein: potential microbes from intestinal tract and toxics ingested or produced by intestinal flora.
Portal streaming: differential blood flow of portal blood from different segments of the intestinal tract, some areas of liver more affected by toxins than others according to the intestine where it was absorbed
-Hepatic artery
-Umbilical vein in neonates
Localization within Kupffer cells
Localization within capillary beds of the wall of gallbladder or arterioles rete of the biliary tree.
Localization within capillary beds of the pancreatic parenchyma
- Biliary: ascending through biliary tree that is in direct contact with duodenum
- Direct penetration: ex: traumatic reticuloperitonitis or foreign bodies. Discrete (focally extensive) or Multiple “layers” involved
Defense mechanisms/Barrier Systems
-Kupffer cell: protects from blood-borne injury. They actively degrade and ingest bacteria and other organisms, senescent cells such as erythrocytes. Antigen presenting cells and particularly important in the removal of endotoxin from portal blood. They migrate and lie sinusoids
-Stellate cells (“Ito” cells): during hepatic injury they alter their morphology and function from storing vitamin A to losing it and initiate hepatic fibrosis by synthesizing collagen and other ECM components. They also participate in the release of growth factors and haptic immune response.
-Reticulin: Sinusoidal scaffold (BM). contains collagen types III, IV, XVIII and extracellular matrix components that support endothelial cells.
Identify the anatomy of the liver.
Describe how the gross and microscopic anatomy play a part into the development of diseases and pattern distribution
The liver is supplied with two sources
- Nutritional blood supply
-Hepatic artery 20-30% blood flow - Functional supply
-Portal vein: 70-80% blood flow
**High source of microbe/toxin exposure
The hepatic vein is the exit of blood from the liver, which enters the caudal vena cava.
Hepatic Lobes is classical functional unit of the liver
-Hexagonal structure 1-2mm wide
-Center: located the central vein, which is a tributary of the hepatic vein
-Portal triads are located at the angles of the hexagon and have portal tracts.
-Portal triads: bile duct, branches of portal vein, hepatic artery, lymph vessels, nerves, all supported by a collagenous stroma.
Divisions of the lobule
-Periportal
-Midzonal
-Centrolobular.
Blood flows always away from central vein toward portal triad
-Portal blood and hepatic arterial blood mix in the sinusoids.
-Blood drains from the sinusoids into the central veins and to progressively larger sublobular veins and then into the hepatic veins.
-Blood and bile flow in opposite directions within the hepatic lobule.
-Kupffer cells: phagocytosis, macrophages of the liver
-Stellate cells: found within the space of Disse, lipid and vitamin A storage, fibrosis (reparative response to injury through myofibroblast transformation and fibrosis)
Pattern of Hepatocellular Degeneration and/or Necrosis
- Random
- Zonal
-Centrilobular
-Paracentral/periacinar
-Midzonal
-Periportal - Bridging
- Massive
Functions of the liver
1. Production and Excretion of Bile
2. Bilirubin metabolism
3. Carbohydrate metabolism
4. Lipid metabolism
5. Xenobiotic metabolism
6. Protein and Urea synthesis
7. Immune function
- Excretory: Production and excretion of bile
- Facilitation of digestion of lipids
3.Provide buffer to neutralize pH of ingesta
-Bile flows in the opposite direction than blood
-Bile formation is continuous, but rate of excretion can vary significantly.
-Bile = water, cholesterol, bile acids, bilirubin (RBC pigment breakdown), inorganic ions.
-Bile acids: synthesized from cholesterol; conjugated to prevent precipitation into calculi. Reabsorbed from ileum, extracted from portal blood, resecreted into bile via enterohepatic circulation (95% recycled). Interruption of process - fat malabsorption and deficiency of fat-soluble vitamins.
-Waste products (excess cholesterol, bilirubin, metabolized xenobiotics) are excreted in bile.
-Bile acids secreted into intestine helps digestion of lipids
-Buffer protects intestine from pH of the stomach.
Cholesterol homeostasis, stimulation of bile flow, intestinal absorption of vitamins, fats.
Xenobiotic metabolism
-Cytochrome P450 enzymes of SER of hepatocytes: major site of metabolism
Protein and Urea Synthesis
-Albumin; variety of transport proteins, lipoproteins, clotting factors, fibrinolysis proteins, acute phase proteins, complement proteins, conversion of ammonia into urea.
Immune Function
-Acute phase proteins kupffer cells, transport of IgA, clotting factors.
Mechanisms of Liver Injury
- Metabolic bioactivation of chemicals via cytochrome P450 to reactive species
- Stimulation of autoimmunity
- Stimulation of apoptosis
- Disruption of calcium homeostasis leading to cell surface bebbling and lysis
- Canalicular injury
- Mictochondrial injury
Diagnose
Acute hepatitis
Chronic hepatitis
Cholestasis
Cholecystitis
Cholangitis
Cholangiohepatitis
Identify
Hepatic necrosis
Icterus
Hyperbilirubinemia
Regeneration
Fibrosis
Biliary hyperplasia
Cirrhosis
Acute hepatitis
-Inflammation of the liver parenchyma.
-Characterized by inflammation, hepatocellular necrosis, and apoptosis.
-Usually requires microscopic evaluation to determine type.
-Involvement depends on cause, response of hosts, and stage or age of lesion.
-Bacterial and protozoal infections lead to accumulation of neurophils.
-Random foci of neutrophilic hepatitis, as consequence of embolic localization of bacteria, relative common in all species.
-Neonates (calves, foals, etc.) E. coli seeds the liver via umbilical veins
-Herpesvirus infections characterized by random distribution of necrosis and apoptosis with minimal infiltrations of lymphocytes. It causes inflammation, vasculitis (blood clots), systemic
-Equine acute hepatitis herpes virus: random white to gray foci of viral -induced lytic necrosis. Salmonellosis, focal necrosis and inflammation.
Chronic hepatitis
-Continued inflammation results in persistence of antigenic stimulus, without stimulus the inflammation would resolve. Characterized by:
-Fibrosis, accumulation of mononuclear inflammatory cells, including lymphocytes, macrophages, plasma cells, and frequently regeneration.
-Neutrophils are often present in unresolved hepatic inflammation such as which characterizes some forms of canine chronic hepatitis.
a. Granulomatous hepatitis: may be focal, multifocal, or diffuse. Focal lesions may not alter hepatic function. (Macrophages, fungus, parasites, foreign bodies, higher order bacteria).
b. Diffuse or severe chronic hepatitis: leads to loss of hepatic parenchyma and architectural distortion. Nodular parenchyma regeneration. This process can lead to end-stage hepatic disease with hepatic failure.
Cholestasis
-Disturbance of the bile flow
-Chronic extrahepatic biliary obstruction and cholestasis leads to extensive fibrosis, which primarily affects the portal triads, then parenchyma.
Cholecystitis
-Chronic or Acute inflammation of the biliary tract or gallbladder can lead to end-stage liver.
-Acute inflammation can result from viral infections such as Rift Valley fever in ruminants
-Infectious canine hepatitis
-Characteristic Edema and hemorrhage in the gallbladder
-Bacterial infectious rising from intestine or derived from blood can be associated
-Chronic associated with prolonged bacterial infections of the biliary tree, parasites, or ongoing irritation from choleiths.
-Rapture of the gallbladder rare, but can lead to peritonitis.
Cholangitis
-Inflammation of the biliary ducts either intrahepatic or extrahepatic.
-Neutrophilic (suppurative) the most common type
-Rapture of affected ducts can lead to hepatic abscesses formation.
-Most due to ascending bacterial infection from the intestine, E. coli, Streptococcus, Bacteroides, Clostridium.
-Lymphocytic cholangitis: mostly cats
Cholangiohepatitis
-Inflammation that affects both the biliary ducts and hepatic parenchyma.
-Most cases intrahepatic disease, usually as an extension of biliary disease
Identify
Hepatic necrosis
Zonal Hepatocellular injury
-Centrilobular (periarcinar), midzonal (between centrilobular and periportal areas), or periportal (centroacinar) areas.
-Accentuation of the normal lobular pattern is evident on the capsular surface of the liver. It is not a specific change, as it may be with zonal hepatocellular degeneration and/or necrosis, passive congestion, or diffuse cellular infiltration of the portal and periportal areas. Often reflecting hepatic involvement of hematopoietic neoplams, such as lymphoma and myeloproliferative disorders.
Icterus/Jaundice
-It is the yellow discoloration of the tissue particularly those with high elastic tissue content, including the sclera and aorta.
-Due to increase bilirubin
Hyperbilirubinemia
-Increase bilirubin in tissue, blood, urine. Increased concentration of conjugates/unconjugated bilirubin in blood.
->0.5 ml/dl but may not be icterus
-Hepatic dysfunction if not the only cause. Other causes can be intravascular mehomlysis
-Horses present icterus with acute hepatic dysfunction, but may or may not occur with chronic hepatic disease.
-“physiologic icterus” in horses that do not eat for several days, the uptake of bilirubin from the plasma by hepatocytes is decreased.
-Example: Canalicular bilirubin in liver from a calf with hemolytic disease caused by Babesios, between hepatocytes are yellow/brown.
-Gilbert syndrome and Dublin-Johnson syndrome in sheep.
Regeneration
-Liver has a remarkable ability to regenerate loss hepatic mass
-As much as 2/3 mass excised experimentally and no loss of hepatic function.
-Compensatory hyperplasia
-Hepatocytes replacement = increase in the size of existing lobules
-Bile ducts epethilium, sinusoids hyperplasia.
-Replacement of hepatocytes from necrosis occurs through ductular reaction
-Involvement of TGF-alpha and HGF
-Regeneration without scarring occurs if no ECM (reticulin) damage or collapse.
Fibrosis
-It can be lethal
-In the normal liver, delicate scaffolding of collagen and other ECM components produced by stellate cells, endothelial cells, and hepatocytes make up a normal framework of the sinusoid. Spatial relationship to the hepatocytes is maintained.
-Change in the type of collagen and their site of deposition
-Overall increase in ECM , up to six times as much collagen type I, III, XVIII.
-Large lipid containing vacuoles in cytoplasm
-Stellate cells activated by chemical injury, biliary obstruction, iron overload.
-Loss of microvilli on the luminal surface of hepatocytes and loss of gaps between epithelial cells.
-Synthetic, catabolic, and excretory functions compromised
-Toxic injury = centrilobular fibrosis, centrilobular hepatocytes are the site of metabolism for most drugs.
-Chronic passive hepatic congestion from long-standing right-side heart failure can cause fibrosis in the centrilobular region.
-Periportal fibrosis from chronic inflammatory condition
-Bridging fibrosis is analogous of bridging necrosis: implies fibrosis that extends from one portal tract to another or to central vein.
-Fibrosis is usually quite extensive before clinical signs of hepatic dysfunction are perceived.
-Migrating nematodes can cause multifocal hepatic fibrosis.
Biliary hyperplasia
-Ductular reaction is the proliferation of bipotential progenitor cells found at the edge of the portal tract at the level of the cholangioles that can eventually mature into bile ducts and/or hepatocytes.
-Basophilic cells (cholangioles) also known as oval cells form poorly defined ducts and tubules with a lack of lumen.
-Ductular reactions can develop as a result of injuries that inhibit proliferation of hepatocytes in CHOLESTASIS and in regions of HYPOXIA.
-Hyperplasia of bile ducts or ductular reaction can occurs swiftly in young animals.
Cirrhosis
-A diffused process characterized by fibrosis and the conversion of the normal liver architecture into structurally abnormal lobules.
-Final, irreversible, end-stage liver term.
-Total absence of any normal lobular architecture
-Formation of fibrous bands and regeneration of hepatic tissue between them leads to the formation of variable sized regenerative nodules.
-Example: phenobarbital for many years, dog liver small, firm, and irregular with nodules of regenerative parenchyma separated by tracts of fibrous connective tissue.
-Lumpy bumpy
-All affects blood flow, often leads to shunting of blood
-Commonly associated with: Chronic congestion, chronic toxins, chronic inflammation, COPPER TOXICITY (Bedlington Terriers).
-Pyrrolizidine alkaloids, drugs such as primidone for dogs.
Identify and describe
Cholelithiasis
-Developmental abnormalities of the gallbladder more common in cats. Bilobed and occasionally trilobed gallbladders occurs. Usually of no clinical significanse
-Biliary atresia: congenital abnormality where the extrahepatic ducts are no patent or absent. It leads to hyperbilirubinemia an jaundice.
-Gallstones: occur infrequently in all animal species.
-Especially ruminants, of no clinical significance unless they migrate and obstruct the extrahepatic bile ducts. Larger gallstones can lead to pressure necrosis and inflammation (cholecystitis)
Cystic mucinous hyperplasia of Gallbladder
-Only reported in dogs and sheep
-No aparent abnormalities until it is opened and drained.
-Affected mucosa is gray-white with a diffusely thickened, sponge-like consistency.
-Sessile or polyp-like masses or large cysts are occasionally found and evident as papillary projections into the lumen.
-Numerous cysts variable in size are hyperplastic 1-3mm distort and thicken the mucosa, containing a copious amount of mucus.
-Usually incidental and of no significance to the host
-Unknown cause
Gall bladder mucocele
-Characterized by distended gallbladder filled with tenacious mucus.
-Signs of biliary obstruction and occasionally associated with thrombosis and gallbladder rapture.
Smaller dog breeds are predisposed
*Shetland sheepdogs
-Mucosal is hyperplastic, the bile duct usually affected and cholestasis develops.
-Uncertain pathology
-Hyperthyroidism and Cushings in dogs may be associated with higher incidence
-Gallbladder filled with jelly-like mucous
Identify patterns of hepatic lesions: random, zonal, acinar, lobular, bridging, massive patterns and their relationship to gross presentation and likely contributing etiologic agents.
Pattern of Hepatocellular Degeneration and/or Necrosis
Recognizing patterns can help with determining differentials
Necrosis and Apoptosis
-The epithelial cells, hepatocytes, and biliary epithelium are the principal targets of most liver diseases.
-Sublethal injury to hepatocytes is characterized by cell swelling (hydropic degeneration), steatosis, or atrophy.
-Material that can not be digested any further is retained as lupofuscin, pigment can be found in affected cells.
-Necrosis exhibits karyorrhexis, swelling, rapture and fragmentation of cell body.
-Coagulative necrosis results from sudden denaturation of hepatocytes and produces swelling with eosinophilic cytoplasm, karyorrhexis or karyolysis.
-Lytic necrosis: loss of hepatocytes and influx of RBCs, inflammatory cells, collagen and ECM.
-Classic apoptosis: TNF-alpha or Fas-ligand, caspase activation. Microscopically formation of apoptotic bodies between hepatocytes, sinusoids or lumen, or macrophages.
- Random: characterized by single cell necrosis or throughout the liver or multifocal areas of necrotic hepatocytes.
-Typical of infectious agents: virus, bacteria, protozoa.
-Lesions may be obvious grossly as discrete, pale or dark red foci that are sharply delineated from the adjacent parenchyma. Size from <1mm to several cm.
-Example: Tyzzer’s disease in horse due to Clostridium piliforme. Salmonellosis, focal necrosis and inflammation, pig, infiltrated by macrophages and form discrete granulomas termed “parathyphoid nodules” within the hepatic lobules H&E stain.
-Bridging degeneration and necrosis
-Massive degeneration and necrosis
-Lobular (entire lobe)
-Acinar: from central vein to central vein. - Zonal: characteristically has an enhanced lobular pattern on the surface of the organ or capsular. Damaged hepatocytes swell in a zone. The portion of the lobule appears pale. Liver pale, with round margins, enlarged, and increased friability. Dilation and congestion of sinusoids and affected zone appears red.
-Centrilobular degeneration/necrosis: particularly common, this portion of the lobule receives the least amount of oxygen/blood, susceptible to hypoxia and it has the most enzymatic activity capable of activating compounds into toxic form. It can result from severe anemia, right side heart failure. Passive congestion of the liver results in hypoxia due to stasis of blood and produces atrophy of centrilobular hepatocytes.
-Paracentral/periacinar: involves a wedge of the parenchyma around the central vein because only the outer margin of one diamond-shape acinus is affected. Typically reflecting the action of toxin that requires bioactivation, severe anemia, or acute anemia.
-Midzonal: unusual lesions in domestic animals but have been reported in pigs and horses with AFLATOXICOSIS and cats exposed to HEXACHLOROPHENE.
-Periportal: uncommon, follows exposure to toxins, such as PHOSPHORUS that do not require metabolism by mixed function oxidases (most active in centrilobular hepatocytes). Some compounds may be metabolized to harmful intermediates by cytoplasmatic enzymes for in periportal hepatocytes, or injury results to the first hepatocytes encountered.
- Bridging: can result of confluence of areas of necrosis. Bridge may link centrilobular areas or to periportal areas.
- Massive: the term describes necrosis of the entire hepatic lobule or contiguous lobules. The gross appearance differs according to the maturity of the lesion.
-Acute cases: majority of parenchyma is affected, liver modestly increased in size with smooth external surface and dark parenchyma due to extensive congestion.
-Regeneration does not occur as a rule because virtually all hepatocytes are affected.
-Microscopically blood filled spaces within connective tissue stroma devoid of hepatocytes.
-Later in the course of the process stellate cells or other ECM producing cells that survive migrate to injury area and contribute collagen I.
-The final result is collapse of the lobule and replacement of parenchyma with scar consisting of condensed stroma, variable amounts and types of collagen.
-Grossly liver appears smaller than normal with a wrinkled capsule
Identify and describe the pathogenesis of
Congenital biliary cysts
-Developmental anomalies that occur in all domestic animals, rare and of little consequence.
-Incidental finding and found in animals of any age.
-Single or multiple cysts filled with clear fluid.
-Think walled cysts, single layer of biliary epithelium.
-Distinguish from parasitic cysts, particularly from cysticerci because they also have thin-walled fluid filled. Larval cestode distinguishing factor.
-Multiple cysts, Polycistic disease: liver, kidney, pancreas +/-, West highland White Terriers predisposed, cats with Persian, goats and lambs.
-Congenitally affected animals can die of either liver or renal failure.
Capsular fibrosis
-Discrete fibrous tags or plaques are frequently present on the diaphragmatic surface of the liver and on the adjacent diaphragm of the horse.
-Larval nematodes migration originally believed to be the cause of this type of lesion.
-Possibly as a result of resolution of nonseptic peritonitis, contact between diaphragm and adjacent liver capsule has been proposed as pathogenesis.
-Numerous white-gray fibrous tags
Acute passive congestion
-Can occur as a consequence of acute right-sided heart failure.
-Appearance differs from chronic congestion
-Persistent centrilobular hypoxia leads to atrophy or loss of hepatocytes and eventually centrilobular fibrosis.
-Fibrous of the central vein (phlebosclerosis) may occur.
-Slight enlargement of liver, blood flows freely from any cut surface. Centrilobular areas are congested, dark red.
Chronic passive congestion
-Nutmeg liver
-The congestion is centrilobular and the peripheral lipid accumulation give the liver a characteristic appearance “nutmeg”.
-Almost always a consequence of cardiac dysfunction.
-Right heart side failure, elevated pressure within caudal vena cava that later involves the hepatic vein and its tributaries.
-It can eventually lead to to fibrosis near central veins, which is termed cardiac sclerosis, and can progress to cardiac cirrhosis, with fibrosis bridging between central veins.
-Morph: hepatomegaly, heart failure related right side.
-Common in aged dogs and secondary to right atrioventricular valve insufficiency resulting from valvular endocardiosis (myxomatous degeneration).
-Diffuse enlargement, rounded edges of liver lobes.
-Oxygen and nutrient depravation
-Sinusoids dilated, congested, and grossly appear red.
-Fatty degeneration (steatosis) = enhanced lobular reticular pattern.
-Liver is firm because of fibrosis, CV surrounded by connective tissue, macrophages containing hemosiderin as a result of erythrocytes breakdown in chronic congestion.
Congenital portosystemic shunts
characteristic lesion is a single anomalous vessel that connects the portal circulation with the systemic circulation, small but normal color liver.
-Congenital: is an abnormal vascular channel that allows blood within the portal venous system to bypass the liver and to drain into systemic circulation. It can be intrahepatic or extrahepatic, but usually limited to one single relatively large-caliber vessel.
-Intrahepatic: typically involves failure of closure of the ductus venous at birth. Vessel conducts blood from umbilical vein to the caudal vena cava. Mostly located in left side of liver and large breed dogs
-Extrahepatic: portal vein to caudal vena cava anastomoses and portal vein to azygous vein anastomoses, occurs in small breed dogs and cats.
Animal develops signs of hepatic encephalopathy
-Hyperammonemia
-Ammonium biturate crystals in urine
-Liver is small, may have absence of portal veins, and lobular atrophy.
-Ascites does not occur because portal vein pressure is normal
Hepatic lipidosis (Steatosis)
Tension lipidosis
-Discrete, pale areas of parenchyma at the liver margins are common in cattle and horses.
-These foci typically occur adjacent to the insertion of a ligament (serosal) attachment, which impedes blood supply to that area and exerts tension on the capsule.
-Affected hepatocytes accumulate fat within cytoplasm (steatosis) as a consequence of hypoxia, no functional significant lesions.
Metabolic Lipidosis
-Lipids are normally transported to the liver from adipose tissue and the GI tract in the form of either free fatty acids or chylomicrons. Within hepatocytes free fatty acids can be esterified to triglycerides, converted to cholesterol or phospholipids. Some oxidation of fatty acids to ketone bodies for energy production occurs within hepatocytes. Triglycerides can be complexed with apoproteins to form low-density lipoproteins, and these are released into plasma as readily available energy source.
-Except for ruminants, the liver also actively produces lipids from amino acids and glucose.
-The presence of excessive lipid within the liver is termed steatosis or lipidosis “fatty liver” occurs when rate of triglycerides is higher than metabolic degradation or release as lipoproteins can process.
-Steatosis or lipidosis can occur as sequela to a variety of perturbations of normal lipid metabolism.
-Example: high fat or carbohydrate diet, increased metabolism of fat, lactation, starvation, endocrine disorder, increase glucose/insulin concentrations.
-Abnormal hepatocyte function that leads to triglycerides accumulation in cells.
-The liver enlarges and becomes yellow
-Lipids can accumulate in different areas such as centrilobular regions in mild to moderate cases
-In severe cases the entire liver becomes greasy texture. Histologically clear round large vacuoles appear displace the nucleus of hepatocytes.
-Swollen with rounded borders, pale, friable (break easy), greasy on cut surface.
-May present early reticular yellow pattern.
-Oil Red O stain
Causes:
-Deficiency in cobalt and vitamin B12 in sheep and goats “white liver disease”
-Toxicity that can not be reversed
-Ketosis is a metabolic disease results from impaired metabolism of carbohydrates and volatile fatty acids. Disorder of ruminants
-Bovine fatty liver syndrome “fatty liver disease” mechanistically similar to ketosis and is specifically common in ruminants with high energy demands, gestation, obesity, right before or after parturition
-Feline fatty liver syndrome idiopathic hepatocellular steatosis in cats, obese, anorexic, hepatic failure.
-Endocrine disorders such as diabetes mellitus and hypothyroidism. Accumulation of lipids is liver in diabetic animals is the result of increased fat metabolism and decreased use of the lipids by injured hepatocytes.
DDx for pale, swollen livers
-Lipid (hepatic lipidosis): hapatocytes contain lipid vacuoles
-Glycogen (steroid induced hepathopathy, diabetes, glycogen storage diseases): hepatocytes contain glycogen and water
-Hepatic amyloidosis: spaces of Disse contain amyloid also basement membrane of other organs.
Glycogen accumulation
-Glucose is normally stored in hepatocytes as glycogen and it is present in large amounts after eating.
-Excessive accumulation of glycogen occurs with metabolic perturbations involving glucose regulation, diabetes mellitus and glycogen storage diseases.
-Secondary to excess glucocorticoids in dogs, Cushings, iatrogenic. NONGREASY
-Pallor, swelling, vacuolated cytoplasms, but poorly defined and nuclei is not displaced to the periphery of cell like in lipidosis.
Hepatic Amyloidosis
-Most species affected.
-It is not a single disease entity but a term used for various diseases that lead to the deposition of proteins that are Beta-pleated sheets of nonbranching fibrils.
-Affected liver is enlarged, friable, pale. Histologically eosinophilic amorphous deposits usually in space of Disse along the sinusoids, but can be found in the portal tracts and within blood vessels.
-Apple green birefringe in Congo red-stained sections viewed under polarized light.
-Primary amyloidosis: AL = amyloid light chains
-Secondary amyloidosis: AA = amyloid A results from prolonged inflammation such as chronic infection or tissue destruction. It is the most common in VetMed
-Serum Amyloid Associated protein (SAA) apoliproteins that is an acute phase protein synthesized by the liver.
-Inherited amyloidosis: Siamese, Oriental cats, Shar-Pei dogs, Abyssinian cats.
-Beta-amyloid: Alzherimer’s also found in dogs
-Iodine stain: fresh tissue dark brown appearance
-Severe cases for example horses, may experience exsanguination due to liver fragility = rapture.
Copper accumulation
-It specially occurs in sheep
-Normally serum copper is bound to ceruloplasmin and the majority of hepatic copper is bound to metallothionein and stored in lysosomes.
-Excess copper like excess iron can lead to the creation of ROS, damage RBCs, oxidative intravascular hemolysis.
-Common sequence of copper toxicosis:
1. dietary excess in ruminants, contamination of pastures with fertilizers, overcorrection of deficiency, mineral blocks that are formulated for cattle but sheep have access to
2. Grazing animals with inadequate concentrations of molybdenum, which antagonizes copper.
3. Hepatotoxic plants containing phytotoxins, usually pyrrolizidine alkaloids such as Heliotropium, Crotalaria, and Senecio species plants. Pyrrolizidine alkaloids inhibit hepatocellular mitosis, necrotic release and uptake by surviving hepatocytes = overload of copper
4. Metabolic disorders: Bedlington terriers autosomal recessive disorder COMMD1, MURR1. Impaired biliary excretion of copper
-Rhodanine staining
Bile pigments
-Hemodiderin: iron containing pigment (blood) derived from ferritin = Golden-brown to dark. Local/systemic excess of iron. Breakdown of RBCs. Hemolytic anemia
-Hemosiderosis: abundant hemosiderin in tissues, but no organ dysfunction
-Hemochromatosis: increased storage of iron with organ dysfunction
Melanin
-Endogenous pigment that is dark brown or black.
-Benign disorder termed Melanosis
-Congenital melanosis occurs in pigs and ruminants and produces variable sized discolorations in the liver
-Acquired melanosis occurs in sheep in Australia due to ingestion of certain plants
Parasite Hematin
-Liver flukes produce very dark excreta that contain a mixture of iron and porphyrin. These excreta produce the characteristic discoloration that occurs in fascioliasis (Fasciola hepatica) and Fascioloides magna in bovine livers.
Ceroid: pathologic yellow-brown pigment similar to lipofuscin associated with peroxidation of fat deposits.
-Observed within fatty cysts formed in severe hepatocellular steatosis.
Lipofuscin
-Insoluble pigment that is yellow-brown to dark brown and is derived from incomplete oxidation of lipids such as those in cell membranes.
-Amounts tend to increase with age. “Wear and tear” pigment
Diagnose infectious causes of hepatitis:
Herpesvirus
-Particularly occur in neonates or fetuses.
-Abortigenic herpesviruses: Equine herpesvirus 1, bovine herpesvirus 1, caprine herpesvirus 1, canine herpesvirus 1, feline herpesvirus 1, suid herpesvirus 1, ILT: Gallid herpesvirus 1.
-Alpha herpesviruses: Cytolytic (random necrosis), variable inflammation, persistent, latent, fast replicating, intracellular nuclear inclusion bodies.
-Infection occurs via several routes including transplacental exposure, passage through birth canal, contact with infected littermates, contact with oronasal secretions from the dam.
-Virus enter through oronasal epithelium, to bloodstream via infected mononuclear phagocytic cells.
-Multifocal, randomly distributed, small <1mm areas of necrosis in several fetal organs, white-grey.
-Affects mostly liver, kidney, and spleen
Infectious canine hepatitis
Liver abscesses (bacterial infections)
-Bacteria reach the liver via portal vein, bile duct, umbilical veins, hepatic artery, ascending infection of the biliary system, parasitic migration, direct extension of an inflammatory process from immediately adjacent tissues such as the reticulum.
-Systematic infections bacteria examples: Salmonella, Yersinia pseudotuberculosis, Trueperella pyogenes (Arcanobacter pyogenes), Fancisella spp., Norcardia asterioides, Actinomyces spp, Campylobacter fetus subspecies, fetus.
-Hepatic abscesses usually occur as a
sequel to toxic rumenitis (Fusobacterium necrophorum) enters the portal circulation. NECROSUPPURATIVE hepatitis, opportunistic bacteria
-Initially focal areas of hepatocellular necrosis and hepatitis that develops into abscesses.
-Cattle: weight loss, decreased milk production.
-Less commonly phlebitis: abscesses encroach hepatic vein or caudal vena cava, mural thrombosis results due to obstruction of outflow, passive congestion and portal hypertension can occur. Detachment of mural thrombi can produce septic thromboemboli that lodge in the lungs.
-Rapture of abscesses can result in fatal septic embolism of the lungs.
-Other bacterial culprits: Clostridium spp, Leptospira spp, E. coli, Mycobactrium spp. Rhodococcus equi, Corynebacterium pseudotuberculosis, Mucor spp fungal infection.
Tuberculosis granulomas
-Mycobacterium bovis, zoonotic, has been eradicated from almost all US. but its occurrence in other countries varies with the effectiveness of control efforts.
-The primary site of disease is the lungs with subsequent dissemination to other organs including the liver.
-Granulomatous inflammation surrounded by fibrous capsule, randomly distributed
Tyzzer’s disease
-Horse liver pic. Random dessiminated 1-2mm red to dark red foci of necrosis due to Clostridium piliforme infection.
-Clostridium piliforme, a gram negative obligate intracellular parasite.
-Most common in foals, but also occurs in calves, cats, and dogs.
-Typically very young or immunocompromised
-After colonization of GI tract, penetrate portal venous vein and enter liver.
-Enlarged, adematous, and hemorrhagic abdominal lymph nodes, hepatic enlargement, presence of randomly distributed, pale foci of hepatocellular necrosis around it, neutrophils and mononuclear cells.
-Elongated bacili gram negative.
-Enteritis, myocarditis
-Warthin starry stain or Gomori’s silver stain.
Leptospirosis
-Gram negative Leptospira.
-Zoonotic, >23 antigenically distinct pathogenic serogroups.
->200 serovars. Each serovar differs with species and organs affected and severity of disease. Many causing IV hemolysis
-Enters mucous membranes/broken skin
-Shed in urine
-Systemic disease/abortions
-Contaminated water, bedding, and soil are common sources of infection, shed in urine.
-Transplacental infection leads to abortions.
-Infection can involve RBCs, liver, kidney, and other organs.
-Intravascular hemolytic anemia can occur with certain serovars, leads to ischemic injury to centrilobular areas.
-Gross lesions: icterus, hepatic hemorrhage, ascites, focal necrosis, centrilobular necrosis, dissociation of hepatocytes = friable liver
-Waarthin Starry Stain.
Bacillary hemoglobinuria
-Acute and highly fatal disease of cattle and sheep that occurs in various areas of the world.
-Can be endemic in regions where Liver Fluke Fascicolla hepatica infections occur.
Clostridium haemolyticum, gram-positive rods causative agent of bacillary hemoglobinuria are ingested and come to reside within Kupffer cells, but they proliferate in areas of low oxygen tension.
-Bacterial spores germinate/proliferate and release exotoxins, including beta toxin phospholipase C, which induces hepatocellular necrosis, intravascular hemolysis, anemia, and hemoglobinuria.
-Grossly lesions are large, sharply delineated from adjacent parenchyma and usually pale surrounded by hyperemic zone. Acute inflammation
Infectious Necrotic Hepatitis
-Clostridium novyi: “black disease” most common in sheep and cattle, but occurs in horses and pigs also.
-Clostridium novyi type B germinate in areas of lowered oxygen tension and release exotoxins that produce discrete foci of coagulation necrosis and hemorrhage within the liver, hemolysis and eventually death of host.
-Migration of liver fluke, parasitic migration tracts present within the liver.
-Diffuse venous congestion and accumulation of fluid in pericardiac sac and pleural peritoneal cavities.
-Zone of intense hyperemia surrounds necrotic foci. Well demarcated areas of necrosis, peripheral neutrophils, gram positive rods
-High fever, death.
Infectious Canine Hepatitis
-Type III hypersensitivity CAV-1 “blue eye” recovering from disease or vaccination related.
-Canine adenovirus 1
-Majority of infections are not lethal.
-Young dogs < 2 years of age are more likely to die than older dogs.
-Viral predilection for hepatocytes, vascular endothelium, and mesothelium.
-Hepatic necrosis and widespread serosal hemorrhage that can affect a variety of organs.
-Oral exposure with infected urine.
-Viremia last 4-8 days, but virus shed in urine for longer
-Initial viral replication occurs in tonsils and produces tonsillitis, can be severe with spread to local lymph nodes and systemic circulation.
-Leukopenia and fever
-Cytolytic and cause necrosis to infected cells
-Lesions widespread petechia and ecchymoses, accumulation of clear fluid in the peritoneal and other serous cavities, presence of fibrin strands on the surface of the liver.
-Corneal edema, immune-complex uveitis “blue eye”
-May lead to DIC
-Microscopic: random and centrilobular necrosis, INIB, neutrophils common even though it’s a virus.
-Liver enlarged and friable, enhanced lobular pattern is sometimes evident.
Feline Infectious Peritonitis
-Mutated feline coronavirus
-Liver often involved (multisystemic)
-Pyogranulomatous vasculitis
-Fatal
-Wet form: type III hypersensitivity
-Dry form: Type IV hypersensitivity
Mycobaterium
Zoonotic bacteria, can occur in domestic animals, dogs southern states
-Granulomas
-Mycobacterium bovis
-Mycobacterium avium-intracellulare complex
-Mycobacterium Phyton molurus: reptiles
-Gross - random granulomas
-Lung/liver
-Acid-fast positive
-PCR.
Parasitic diseases
(nematodes, trematodes, cestodes)
-Ascarium Suum -Nematode: “milk-spotted liver” diaphragmatic surface of liver in pigs, migration tracts of the ascarid larvae and in adjacent portal areas. The tracts are replaced with connective tissue eventually into fibrous cars which are prominent in the capsular surface. Occasionally abscesses or granulomas.
-Strongylus spp in horses
-Stephanurus dentatus in pigs
-Calodium hepaticum in dogs and cats
-Dirofilaria immitis: occasionally develop vena caval syndrome, a.k.a postcaval syndrome. Typically occurs in dogs characterized by DIC, intravascular hemolysis, and acute hepatic failure.
-Starts with reticular pattern
-Theories suggests hypersensitivity to antigens released by the worms
Cestodes
-Develop into parasitic Cysts
-Taenia hydatigena: dogs. Adult cestodes inhabit GI tract of carnivores and usually innocuous to their DH. Ova ingested can develop into embryos, which penetrate the wall of the gut and then distributed via the blood to any site in the body.
-Cysticercus tenuicollis: horses, ruminants, pigs. Immature cysticerci migrate in the liver and can induce extensive damage of infection is heavy. Comparable to Fasciola hepatica.
-Echinococcus granulosus: dogs, sheep, cattle. Hydatid liver disease, cysts develop, proglottids excreted in feces.
Trematodes
Ruminants
-Fascicolidae: Fascicola hepatic sheep and cattle. Leaf-shape adults.
-Swampy areas suitable for survival of aquatic snails, IH.
-secondary Clostridial disease (perfect anaerobic environment) Clostridium haemolyticum, clostridium novyi.
-Metacercaria ingested by ruminant host and penetrates wall of duodenum to enter peritoneal cavity and liver. Migrate and take residence in the bile ducts. Hemorrhagic tracts of necrosis, liver parenchyma dark red tracts, acute inflammation, later become pale.
-Dirocoelidae
-Opisthorchidae
Dogs: Heterobilharzia americana - shistosome
-Granulomatous lesions (liver, mesentery, pancreas, more)
-Fascicola magna: adults parenchyma, North America, Elk and white-tail deer.
-Fascicola hepatica: adults in bile ducts.
Fungal
Ruminants
-Aspergillus
-Zygomycetes
Systemic fungi
-Blastomyces dermatiditis
-Coccidiodes immitis
-Histoplasma capsulatum (very small circular): endemic in US and Canada. Dogs affected most often. Inhalation or ingestion. Pulmonary infections become disseminated. Multifocal distribution of granulomas with intralesional yeast form of the organism. Yeast in cytoplasm of macrophages.
-Cryptococcus neoformans
Staining: PAS, GMS, Mucicarmine
Diagnose toxicities of the liver:
Blue-green algae
Pyrrolizidine alkaloid- containing plants
Cycads
Aflatoxin
Phomopsins
Mushrooms
Sporidesmin
Xylitol
Phosphorus
Metals
Therapeutic drugs
Centrilobular hepatocytes a double whammy!
-Prone to injury from toxins: Uber metabolically active cells (CP450 system)
-Metabolites to more toxic meatbolites
-Prone to injury from blood flow: hear failure, flow compromised. Central location, last to receive blood.
Reticular pattern in liver
-Not specific for any disease, but gives insight!
-Does not have to be centrilobular, just same place in the lobules or other lobules have the same lesion.
-Early on in hepatomegaly the liver may have had the reticular pattern.
Reticular vs. Nutmeg liver pattern
-Main difference in chronicity
-Nut meg common with chronic passive congestion
Diagnose toxicities of the liver:
Toxins love the liver because of its dual blood supply
Cyanobacteria
Blue-green algae
-Cause lethal poisoning in livestock and less common in small animals.
-Late summer or early fall blooms that are dead or dying release preformed toxins such as microcystin LR, a cyclic heptapeptide accumulates in the surface of water and is ingested by animals. It binds to phosphatases 1 and 2A causing hyperphosphorylation of cytoskeletal proteins, ultimately cell death.
-Hemorrhage and necrosis (GI, liver)
-Diarrhea, prostration, death.
-Red swollen hemorrhagic liver. Centrilobular or even massive hepatic necrosis.
-Surviving animals may have chronic liver disease
-+/- sinudoidal endothelial necrosis.
Pyrrolizidine alkaloid- containing plants
**Ingested alkaloids are converted to pyrrolitic ester by hepatic cytochrome 450 enzymes. These esters are alkylating agents, which react with cytosolic and nuclear proteins and nucleic acids.
-Senecio, Cynoglossum, Amsinckia, Crotalaria, Echium, Trichodesma, and Heliotropium generas.
-Mostly chronic intoxication
-Megalocytosis (hepatocytes with enlarged nuclei, antimitotic effect prevent cell division but not nucleic acid division), hepatic fibrosis, biliary proliferation, and nodular regeneration of parenchyma.
-Pigs>cattle>horse>sheep, goats.
-Fibrotic liver
-Characteristic histologic features: enlarged hapatocytes, fibrotic and sometimes distorted liver with an irregular capsular surface. “Megalocytes”
Cycads: contain cycasis, macrozamin - deconjugated by intestinal bacteria = toxic metabolite = methylazoxymethanol
-Liver, GI, neurotoxin
-After absorption in to portal vein, compound yields alkylating agents, leading to acute or chronic liver injury.
-Centrilobular necrosis or hepatocellular megalocytosis caused by mitioinhibitory effects of alkylating agents. Nuclear hyperchromasia and varying degrees of hepatic fibrosis.
-Neurotoxin Beta-methylamino-L-alanine (BMAA).
-Progressive proprioceptive deficits in the hind legs of cattle “dying back”
-Acute toxicity most common in sheep, dogs can also be intoxicated
Cholestatic Plant Intoxicants
-Photosensitization common sequelae. Unknown toxin
-Lantana camara shrub produces toxic pentacyclic triterpenes - lantadene A, B, C. that produces syndrome of chronic cholestasis in grazing animals.
-Bile accumulation evident within canaliculi, hepatocytes, and kupffer cells.
-Brassicca spp. plants: (turnip, kale, rape) cholestasis and secondary photosensitization.
-Microscopically Cholangiectasis, peribiliary fibrosis.
-Secondary photosensitization and icterus can occur in all as the result of impaired bile secretion
Mycotoxins: secondary metabolites of fungi the reproduction is not necessary for survival of the fungus.
Aflatoxins: Aspergillus flavus = aflatoxin B1. Most common, most potents, carcinogenic, teratogenic effects
-Corn, peanuts, cottonseed, commercial dog food.
-Cytochrome P450 toxic intermediates binding to DNA, RNA, or proteins.
-Susceptibility pigs>dogs>horses>calves>birds (ducts, turkey)>adult horses>adult cattle.
-Firm, pale liver, steatosis and necrosis of hepatocytes, biliary hyperplasia, centrilobular bridging fibrosis, cellular atypia (lacking uniformity), hepatocytes megalocytosis.
-Acute aflatoxicosis in dogs characterized by hemorrhagic central to massive necrosis. Steatosis and biliary proliferation also may occur.
Phomopsins
-Fungus Diaporthe toxia, grows on Lupine plants
-Cattle, sheep, horses
-Chronic: atrophic, fibrolytic liver
-Diffuse, scattered hepatocyte necrosis with a background of mitotic figures. Biliary hyperplasia dominate later stage.
-Signs of hepatic failure include photosensitization
-Mycotoxicosis is different than lupines causing lupinosis where no hepatic involvement is present.
Mushrooms
-Aminita spp. and others.
-cyclopeptides
-Small liver, chronic liver massive necrosis, steatosis, hemorrhage. shrunken liver due to loss of hepatocytes
-Death from liver failure 3-4 days
Sporidesmin
-Fungus Pithomyces chartarum grows in dead ryegrass.
-Toxin concentrated in the fungal spores
-Sheep and cattle ingest toxin
-Toxin secreted into biliary tree and produces necrosis of the epithelium of large intrahepatic and extrahepatic biliary ducts with minimal inflammation.
-Cholestasis failure to excrete phylloerythrin frequently leads to photosensitization with skin lesions predominantly in the head.
-Facial eczema.
-Left lobe of the liver (increased proportion of blood draining from SI) most severely affected
-Atrophy and fibrosis “boxing glove” live
Xylitol
-Artificial sweetener prevents oral bacteria from producing acids that damage the surfaces of teeth.
-Acutely toxic to dogs 0.5g/kg
-Hyperinsulinemia, hypoglycemia, icterus, and liver failure
-Chronic liver or midzonal to massive necrosis, periportal vacuolar degeneration.
-Vomiting, lethargy, weakness.
-Theory association with ATP depletion
Phosphorus
-Red phosphorus
-White phosphorus: rodenticide. Unclear mechanism, apparently direct toxicity.
-Gastroenteritis and steatosis of hepatocytes and periportal necrosis because it does not require metabolic transformation by cytochrome P450 enzymes, which are mostly concentrated in the centrilobular region.
Metals
-Excessive iron supplementation = hemonchromatosis. Piglets iron-dextran at birth to prevent anemia, and foals iron poisoning. Massive hepatic necrosis, hyperplasia of bile ducts.
-Copper:
-Hepatosis dietetica (vit E/Sel deficiency)
Therapeutic drugs
MANY!
-Cats deficient in hepatic glucuronyltransferase = acetaminophen toxicity
-Carprofen (varies among canine breeds): occasionally causes acute hepatic necrosis in a variety of dogs, Labrador Retriever more affected.
-Anticonvulsants: primidone, phenytoin, phenobarbital (dogs) chronic liver toxicity
-Liver injury usually occurs when overdoses are ingested
-Site of hepatic injury typically centrilobular
-Diazepam can cause acute fatal hepatic injury in some cats.
Diagnose
Equine serum hepatitis in horses
-Occurs in horses that have received an injection of a biologic that contains equine serum, for example: equine antisera such as tetanus antitoxin or pregnant mare serum gonadotropin.
-Possible infectious etiology
-Fast clinical course and death
-Hepatic encephalopathy, icterus
-“Dish rag” liver: massive necrosis (loss of structural integrity)
-Intravascular hemolysis occurs in the terminal stage
-Liver typically small, flabby, discolored greenish brown to dark brown.
Hepatosis dietetica in pigs
-Vitamin E/ Selenium deficiency
-Free radical (oxidative damage) leads to necrosis
-young rapid growing pigs
-Centrilobular to massive necrosis
Chronic hepatitis in dogs
Differentiate
Nodular hyperplasia
Regenerative nodules
Hepatocellular adenoma
Hepatocellular carcinoma
Cholangiocellular adenoma
Cholangiocellular carcinoma
Lymphoma.
Differentiate
Cholelithiasis Cholecystitis
Cystic mucinous hyperplasia
Gallbladder mucocele
Hepatic Neoplasia (just a few)
-Primary neoplasia: arising from liver. Hepatocellular adenoma can be confused with nodular regeneration grossly. Benign neoplasm. Usually single unencapsulated, variable sized, red or brown masses that compress adjacent parenchyma. Looks like carcinoma. They can arise in livers with no background of abnormality.
-Adenomas are characterized by only one or very few portal tracts, whereas hyperplastic nodules retain normal lobular architecture elements, although the portal tracts are more separated than normal.
-Metastatic neoplasia (very common)
-Hepatocellular carcinoma: malignant neoplasms of hepatocytes. Occur more frequently in ruminants, particularly sheep and dogs. Typically friable, grey to white or yellow to brown tissue, subdivided into lobules by multiple fibrous bands. Mitotic figures, atypia and compressed hepatocyte useful indicators of malignancy.
-Lymphoma: usually metastasized from another organ
-Hemangioma/sarcoma
-Melanoma
Biliary Neoplasia
-Cholangiocellular adenoma: biliary epithelium neoplastic cells. Biliary cystadenoma (a variant)
-Cholangiocellular carcinoma: biliary epithelium neoplastic cells. Umbilicated lesions. Metastasis common
Hepatocellullar Nodular Hyperplasia
-Common in dogs >6 years old increased incidence without predilection for sex or breed
-Nodules can be seen on the capsular surface are typically raised and hemispherical, yellow to tan (although they can be dark red when congested), 0.5 to 3cm in diameter and are more friable than the normal liver.
-On incision they are well demarcated from normal parenchyma and usually compress adjacent parenchyma.
-They contain elements of the normal liver but the lobular pattern is distorted. Increase number of hepatocytes with decrease number of portal tracts and veins.
-Hepatocytes frequently contain cytopalsmic lipid or glycogen containing vacuoles.
Hepatic lymphoma, metastatic neoplasms
The liver and the lung are the two most common sites for metastatic spread of malignant neoplasms. Evaluate if extrahepatic site might be the primary neoplasm and not of liver origin
Malignant lymphoma is the most common metastatic neoplasms found in the liver
-Multiple pale grey-white foci caused by filtrating neoplastic lymphocytes.
-Melanoma: metastatic neoplasm frequently black due to the presence of melanin.
-Hemangiosarcomas are usually dark to red brown because of blood.
Intrahepatic Biliary Neoplasia
-Cholangiocellular (bile duct) adenoma: uncommon in most species. They are usually discrete, firm, and gray or white masses consisting of well differentiated biliary epithelium. They are gland-like structures formed by tubules lined with cuboidal epithelium and moderate amounts of stroma. Tubules may be narrowed and distended from fluid forming cystic structures (cystadenoma). Biliary cystadenoma Congenital are multiloculated and can involved an extensive part of the liver.
-Cholangiocellular (bile duct) carcinoma: malignant neoplasms of biliary epithelium, which usually arise from the intrahepatic ducts, but extrahepatic bile ducts can be affected. They occur in all species.
Typically firm, raised nodules often with central depression (umbilicated) pale gray to tan, and uncapsulated. Metastasis is common. Poorly differentiated carcinomas are composed of packets, islands, or cords, and areas of squamous differentiation can occur. The epithelial components are usually separated by fibrous connective tissue. Cholangiocarcinomas are characterized by multiple sites of local invasion by tumor cells of surrounding hepatic parenchyma.
Chronic hepatitis in dogs
-It is poorly understood
-Progressive course of inflammation and fibrosis
-Some hypothesized that is caused by Leptospira, CAV-1 immune mediated, toxin or drug related.
-Excessive copper retention is best characterized and most common recognizable cause of chronic hepatitis in dogs.
-Liver usually small, often with accentuated lobular pattern, architectual distortion from coarsely nodular to end-stage liver.
-Portal or periportal mononuclear cell inflammation, intrahepatic cholestasis and fibrosis
Cardiovascular System
-Left ventricle
-Left atrium
-Aorta
-Systemic circulation, arteries of each organ
-Vena cavae
-Right Atrium
-Right ventricle
-Pulmonary arteries
-Lungs
-Pulmonary veins to Left heart side
Anatomy of the Heart - review
Pericardial Sac
-Fibrous pericardium
-Parietal Pericardium
-Pericardial space (serous cavity): inner layer, mesothelium.
-Epicardium, visceral layer.
Fatty connective tissue
Myocardium
Endocardium
Trabeculae: Charade tendinae
Cardiac blood supply: left and right coronary artery, which arise from aorta at the sinus Valsalva behind the left and right cups of the aortic valves.
Atria/ventricules and valves
Conduction: SA/AV nodes, bundle of His, right/left bundle branches location important for cardia arrhythmias
Major vessels and structures
-vena cava, pulmonary artery, pulmonary vein, aorta.
-Right atrium/auricle, right ventricle, left atrium/auricle, left ventricle.
-Tricuspid valve, pulmonic semilunar, mitral, aortic semilunar.
-Lymphatics
Sequential contraction: systole
Relaxation: diastole
Conduction system: SAN, AVN, AV bundle
SAN pacemaker
-Sinoatrial node: at the junction of the cranial vena cava and right atrium
-Atrioventricular Node: above the septal leaflet of the tricuspid valve (right AV valve)
-Atrioventricular Bundle: transversing the lower atrial septum onto the dorsal portion of the muscular inter ventricular septum.
-Right and left branches to Purkinje fiber network.
Fetal Heart Anatomy and Congenital Malformations
- Diagnose congenital disease of the heart
-Foramen ovals: Fossa ovals between left and right atrium
-Blood flow/embryology
Malformations
-AS: Aortic stenosis
-ASD: Atrial Septal Defect
-PDA: patent ductus arteriosus
-PS: pulmonic stenosis
-VSD: Ventricular septal defect.
Tetralogy of Fallot
-Pulmonic/Aortic stenosis
Congenital Malformations (in utero)
-If you find ONE abnormality chances are there is MORE
-Just because you can’t see it, doesn’t mean it is not there
-Just because it is a lesion, does not mean it is always pathologic or significant
Causes:
-Toxins, hereditary, microbes, etc.
-Early signs of cardiac failure include: poor exercise tolerance, cyanosis, and stunted body growth
Ectopia Cordis
-Heart formed outside the thoracic cavity
-In cattle, heart has been found subcutaneously in the caudoventral neck area.
Categories
- Defects that cause volume overload: Patent Ductus Arteriosus, Ventricular Septal Defect, Atrial Septal Defect, and Endocardial Cushion Defect.
-Defect between left and right cardiac compartments leads to flow of cardiac flow according to pressure gradient from left side (high pressure) to right side (low pressure).
-Blood shunting consequences is overloading low pressured pulmonary circulation, increased volume left side after entering the lungs.
-Eccentric Hypertrophy of the left ventricle and Atrium to accommodate the increased volume.
-Valvular regurgitation, mitral and tricuspid valve, aortic and pulmonary valves insufficiency.
-Progressive Atrial dilation - Cause Pressure overload: ventricular outflow obstructions result in progressive and chronic increase in intraventricular pressure.
-Pulmonic and Aortic Stenosis, Coarctation and interruption of the aorta.
-Cocentric ventricular hypertrophy that eventually results in a diastolic failure. - Cause Cyanosis: Non-oxygenated blood from right cardiac compartment flows to left compartment or bypasses the left compartment and flows directly into the systemic circulation.
-Tetralogy of Fallot, Pulmonary to Systemic blood shunting (some VSD, PDA) Tricuspid Atrasia/right ventricular hypoplasia, double-outlet right ventricle, transportation of the great vessels, etc. - Miscellaneous cardiac and vascular defects:
-PPDHS (peritoneopericardial diaphragmatic hernias), Persistent right aortic arch (PRAA), Endocardial Fibroelastosis, anomalous pulmonary venous return, double aortic arch, retroesophageal left subclavian artery, valvular hematomas, and situs inversus.
Interventricular Septal Defect
What is the number 1 top defect of bovines?
Below the valves, high and low
Atrial Septa Defect
Above the valves
VSD Interventricular Septal Defect
-Failure of complete development of intraventricular septum
-Below the aortic valves on the left
-Left to right shunt initially but can also be right to left
-Right ventricular hypertrophy (right defect)
-All domestic species
-Top heart defect of bovines
-Dogs: English bulldog, English Springer Spaniel, West Highland white terrier.
-More commonly in the upper inter ventricular septum, below the aortic valves (on the left)
-Bronchopneumonia, pulmonary edema, serous atrophy of fat, cardiomegaly.
Atrial Septal Defect
-It could represent the failure of closure of the foramen oval, which is an interatrial septal shunt that allows blood to bypass the lungs of the fetus, or it can be result of true septal defects at another site because of faulty development of interatrial septum.
-Doberman pinscher, and Samoyed.
-Modled, tan pink and dark red.
-Left to right shunt but can also be right to left
-Patent foramen ovale
-All domestic species
Tetralogy of Fallot
-Four lesions:
1.Ventricular septal defect located high in the septum
2. Pulmonic Stenosis
3. Dextroposition of the aorta (overriding aorta)
4. Hypertrophy of the right ventricular myocardium.
-Increased pressure in the right side that shunts unoxygenated blood from hypertrophic right side to the underdeveloped left side
-Results in systemic hypoxia and secondary polycythemia
-Shunts right sided blood to the left
-Blood bypasses lungs back into circulation
-Hypoxia, polycythemia, cyanosis
-All domestic species
-Dogs: Keeshond (inherited) English bulldog.
Pulmonic Stenosis
-Inherited in Beagle dogs, Basset hound, boxer, Chihuahua, Chow Chow, Croker spaniel, English bulldog, Labrador retriever, Mastiff, Newfoundland, Samoyed, Schnauzer and Terrier.
-Narrowing of the Pulmonary valvular area
-Several lesions: formation of circumferential valve with small central orifice in a dome of thickened valvular tissue.
-Coronary artery obstructs the right ventricular outflow tract in English bulldogs.
-Pressure overload, right ventricle hypertrophy (concentric)
-Hepatic congestion, chronic passive congestion
-Irregular intimal thickenings (jet lesions)
-+/- C/S: exercise intolerance, collapsing, arrhythmias, heart failure.
Aortic Stenosis
-True aortic stenosis is uncommon
-Subaortic stenosis: frequent (dogs and pigs)
-Dogs: any large breed
-Bull terriers, boxers, Newfoundland, German Shepherds, Shorthair pointers, Goldens, Great Dane, Roots, Samoyed.
**Pulmonary congestion, cough, spit up blood.
-A thick, white, broad band of fibrous connective tissue encircles the left ventricular outflow tract (LVOT) below the aortic valve. The force of the blood ejected through the stenotic less is responsible fore the “jet lesions” in the overlying aorta.
-Sometimes mild and limited to white nodules on the ventricular septum immediately below the valve.
-Microscopically: loosely arranged elastic fibers, collagen fibers mixed with fibroblasts and chondrocytes-like cells.
Patent Ductus Arteriosus
&
Peritoneopericardial diaphragmatic hernias
-Poodle, Collie, Pomeranian, Chihuahua, Crocker spaniel, English springer spaniel, German shepherd, Keeshond, Maltese, Yorkshire terrier, Bichon fries, Shetland sheepdog breeds.
-Poodles: inherited polygenic trait, Females higher incidence.
normal post embryologic transformation: ligaments arteriosum
-left to right shunting (more pressure in left)
-How long does it take to close normally? it varies, fairly quickly within hours, day or two.
-Junction between pulmonary artery and the aorta.
-Fetus: most blood bypasses lungs and goes to body.
Peritoneopericardial diaphragmatic hernias (PPDHs)
-Incomplete development of diaphragm
- Abdominal viscera herniates into the pericardial sac
-Dogs/cats: Persians
-Ischemic necrosis
-They are rare but most common congenital pericardial anomaly in cats.
-PPDHs results from defective separation of the developing liver and the septum transversum, mental fat may fill the pericardial cavities and compress the heart. Parts of the liver are often incarcerated in the pericardial sac and compress the heart.
-Intrahepatic myelolipomas can develop.
Persistent right aortic arch
-German shepherds, Irish setter, Great Dane dogs predisposed
-Right 4th, left ductus arteriosus, pulmonary artery form ring around esophagus and trachea
-Esophageal compression is relieved by dividing the ductus (or ligaments arteriosum)
-Clinical presentation and sequelae: Aspiration pneumonia.
-Right 4th aortic arch (instead of left) develops and ascends on the right side of the midline so that the ligaments arteriosum forms a vascular ring over the esophagus and trachea.
-Eventually esophageal obstruction and proximal dilation megaesophagus
- Diagnose right and left sided heart failure. Diagnose and describe the pathogenesis (pathophysiology) of lesions of other organ involvement.
Postmortem Changes
-Chicken fat clot: not pathologic. The clot forms to the shape of the lumens of the vessels from which it was removed. It consists primarily of clotted plasma and fibrin and other coagulation cascade proteins. Erythrocyte sedimentation, separation can occur in all animals but horses most susceptible, high erythrocyte sedimentation rate. Pale white to yellow or shiny red or mixture.
-Euthanasia solution: gritty blood, brownish sludge in the ventricle. Focal hemorrhage and discoloration intracardiac injection.
Dysfunction/Responses to injury
-Pump failure: weak contractility and emptying of chambers, impaired filling
-Obstruction of forward blood flow: valvular stenosis, vascular narrowing, systemic or pulmonary hypertension
-Regurgitation blood flow: volume overload of chamber behind failing affected valve
-Shunted blood flows from congenital defects: septal defects in heart, shunts between blood vessels
-Rupture of the heart or a major vessel: cardiac tamponade, massive internal hemorrhage
-Cardiac conduction disorders (arrhythmias): failure of synchronized cardiac contraction.
- Diagnose myocardial degeneration,necrosis and mineralization. Provide differentials diagnoses based on species and history.
- Identify hemorrhage in the heart and list possible causes.
H—Hyperparathyroidism, Humoral hypercalcemia of malignancy, Houseplants
A—Addison’s disease; Aluminum or vitamin A toxicity
R—Renal disease, Raisins (Grapes)
D—Vitamin D toxicosis
I—Idiopathic (particularly in cats; very rare in dogs)
O—Osteolytic
N—Neoplasia (humoral hypercalcemia of malignancy)
S—Spurious
Cardiac Adaptation to injury
-Very limited!
-Atrophy/hypertrophy
-Fatty degeneration
-Necrosis/apoptosis
-Hyperplasia: only in very young animals, then no more!
Compensatory Mechanisms
-Cardia dilation: to increase contractile forces, and increase stroke volume
-Myocardial hypertrophy: due to increased pressure or volume overload
-Increased heart rate
-Increased peripheral resistance
-Increased blood volume
-Redistribution of blood flow
Heart failure
-If it is long enough.. results are the same
-Impaired pumping/filling: impaired ventricular ejection (systolic function) impaired venous return (impaired filling -diatolic failure) heart failure.
-Can be due to either or both
Pathophysiology of Heart failure
-Right-sided: signs of congestion in the systemic circulation, Ascites and peripheral edema
-Left-sided: signs of congestion in the pulmonary circulation, pulmonary edema, dyspnea.
-Bilateral: in small animals = pleural effusion is usually associated.
-ANY type can be associated with cardiac dilation and or hypertrophy.
Most common cardiac diseases
-Horses: Fibrinous pericarditis, Toxic cardiomyopathy (ionophores, white snakeroot), Endocardial fibrosis and calcification, Endocarditis
-Ruminants: White muscle disease, Cardiotoxcicity (ionophores, gossypol, Cassia Occidental’s, Karwinskia humboldtiana), Brisket disease (high altitude disease), Pericarditis, Endocarditis, Malignant lymphoma.
-Pigs: Mulberry heart disease (Vit E deficiency), Pericarditis, Endocarditis.
-Dogs: Myxomatous valvular degeneration (calcular endocardiosis) , Congenital heart disease, Dilated cardiomyopathy, Hemorrhagic pericardial effusion, Cardiac neoplasia, Dirofilariasis.
-Cats: Hypertrophic cardiomyopathy, Dilated cardiomyopathy, Hyperthyroidism-associated hypertrophy, Congenital heart disease.
Disturbances of Circulation
-Hemorrhage: trauma (physical injury) = myocardial hemorrhage,
Tears and raptures of tissue resulting from loss of structural integrity attributable to invasive and destructive properties of neoplasms. Stretching, tearing, lacerating or crushing blood vessels int theses structures, penetrating wounds, lacerations, or fractures bones, shear forces of trauma. Hemangiosarcomas destructive properties.
-Epicardial Hemorrhage: all animals.
Agonal/anoxia (Equine also have endocardial hemorrhages with this)
Septicemia, endotoxemia, electrocution with edema, Vita/Sel deficiency.
Canine: viral morbillivirus (canine distemper), parvovirus. Parasitic: N. canine, T. cuzi, T. gondii. Rickettsial: R. rickettsia, E. canis, Bartonella elizabethae. Spirocheatal: Borrelia birgdorferi. Fungal/Algea: Prototheca sp.
-Pigs: Mulberry disease. Myocardial hemorrhage and degeneration/necrosis, diffuse, severe, heart. Cause: selenium deficiency aka dietary microangiopathy. Gossypol: cottonseed pigment (also toxic to equine), encephalomyocarditis virus. Massive hepatic hemorrhage also occurs with vitamin E deficiency. Red and pale mottled areas of hemorrhage and necrosis in heart.
-Pericardial Dilation: The pericardium responds to excess fluid in the pericardial space by dilation. Requires adequate time to adjust in size.
Hemopericardium = blood rapidly fills the pericardial cavity and death occurs unexpectedly from CARDIAC TEMPONADE (a condition with compression of the heart by blood leading to reduced CO).
Hydropericardium: is the accumulation of clear, light yellow, watery, serous fluid (transudate) in the pericardial sac. In cases associated with vascular injury, few FIBRIN strands are present, and the fluid may clot once exposed to air. Congestive heart failure associated with generalized edema, ascites, hydrothorax, hydropericardium.
Dz: ascites syndrome of poultry, pulmonary hypertension (Brisket disease), renal failure, hypoproteinemia. Septicemia in pigs, Ruminants (“heart water” Cowrie ruminantium infection), African horse sickness, and Bovine ephemeral fever.
-Effusions: Transudates, think mechanisms of edema. Exudates
Morphologic dx: Submandibular edema and pectoral edema secondary to Congestive heart failure.
Etiologic Dx: PIMELEA spp. toxicity or high elevations and hypoxia.
Dz name: Brisket disease.
-Lymphangectasia: puppy with congenital lymphedema: lymphatic hypoplasia/aplasia. Example: epicardium of young horse, tortuous appearance of the epicardial lymphatic vessel, which fails to make connections with other vessels or are obstructed because of anomalous development.
-Thrombosis and embolism
-Cell death and degeneration: Most frequent sites of focal lesions: left ventricular papillary muscles, subendocardial myocardium, especially when related vascular perfusion issues.
-Myocardial Necrosis and mineralization:
Ionophores: monensin, lasalocid (Equine, canine, low doses kills!). White snakeroot = tremetol toxin (equine). Oleander, Blister beetle. Increases the concentrations of intracellular calcium and possibly sodium.
Other animals: Selenium deficiency, carcinogenic plants (Vit D toxicity), Potassium, copper, thiamine, magnesium deficiency. Brain heart syndrome (dogs). Anthracycline toxicity in dogs, and gossypol toxicity in pigs.
-Neurogenic cardiomyopathy (heart-brain syndrome) dogs: Necrosis. syndrome in dogs characterized by unexpected death 5-10 days after diffuse CNS injury (hit by a car). Affected dogs die of cardiac arrhythmias caused by myocardial degeneration and necrosis. Myocardium numerous coalescing pale white streaks and poorly defined areas of myocardial necrosis, most often involving the papillary muscles of left ventricle. Concentrated in the inner half of LV.
-White muscle disease: degeneration/necrosis depends on the severity of damage. Many die acutely of cardiac failure. Early deaths: necrosis-related arrhythmias when cardiac conduction is disrupted. Die with cardiac dilation, scarring, and lesions of chronic congestive heart failure.
-Endocardial mineralization: Fibrosis with or without mineralization occurs in chronically dilated hearts, in hearts with “Johne’s disease” cause of mineralization is unknown, but thought to be metabolic disturbance related to dysfunction of macrophages (via D analog maybe?).
Rabbits Vit D toxicity Ddx HARDIONS.
-Pericarditis: inflammation of the pericardium is frequently seen with bacterial septicemias and typically results in fibrinous pericarditis. Grossly, both visceral and parietal pericardial surfaces are covered by variable amounts of yellow fibrin deposits, can result in adherence. Example: horses with Streptoccocus equi. infection. When survival is prolonged, surface fibrous organization of the exudate.
-Suppurative pericarditis: cattle with complications from traumatic reticuloperitonitis (hardware disease). Infection and septicemia is introduced, congestive heart failure after weeks or months.
-Neoplastic transformation. Exposed parietal surfaces are thickened by fibrous connective tissue and covered by fibrinopurulent exudate. Heart sounds are muffled. Interfere with cardiac filling thus CO.
-Embryologic defects
-Hypertrophy:
-Physiological Atrophy
-Serous atrophy
-Neoplasia: cardiac hemangiosarcoma (HSA) is an important neoplasm of dogs and can rise either in the heart (primary) or via metastasis such as from the spleen. Grossly protruding red-to red-black blood containing masses are located on the epicardial surface and may protrude into the lumen of atrium. Rapture can cause hemoperricardium and cardiac tamponade. Factor VII-related antigen CD31 endothelial marker
-Inflammation: Lymphocytic myocarditis is usually a lesion of viral infections. Example: parvovirus infection in puppies. Generalized lesions result in acute congestive heart failure. The heart is pale flabby, and disseminated interstitial lymphocytic infiltrations, scattered myocytes with large basophilic, intranuclear viral inclusion bodies in dogs that survive fibrosis.
Trypanosome cusi: fatal chronic myocarditis, dogs < 1 year old. Ascites, lymphadenomegaly, hepatomegaly. Heart multiple yellow-white myocardial streaks and spots accompanied by hemorrhage. Right-sided congestive heart failure.
- Differentiate, diagnose and list differentials for myxomatous valvular degeneration (endocardiosis) and vegetative valvular endocarditis.
Vegetative Valvular and Mural Endocarditis
-Endocarditis is usually the result of bacterial infections, except for lesions produced by migrating Strongylus vulgarism larvae in horses and rarely in mycotic infections. Grossly the affected valves have have large, adhering friable, yellow-to-gray masses of fibrin termed vegetations, which can occlude the vascular orifice. In chronic lesions the fibrin deposits are prganized by fibrous connective tissue to produce irregular nodular masses termed verrucae (wart-like lesions). Mitrial>aortic>tricuspid>pulmonary.
Affected animals often have pre-existing extracardiac infections, such as mastitis, hepatic abscesses, dermatitis, more than one bout of bacteremia. Turbulent intracardiac flow associated with congenital abnormalities may contribute to initiation of lesion.
-Virchow’s triad important in thrombogenesis: endothelial injury, turbulence, hypercoagulatbility.
Lasagna or endocarditis
-Eetiology: many, mostly bacteria, fungi, parasite in equine.
-Hidden bacterial colonies in his-towpath
-Dull, irregular, friable, fibrosis chronic.
Staph, Strep, common cause in all species
-Dogs and cats: E. coli, Bartonella.
-Cattle: Trueperella pyogenes, most commonly bacteria.
-Horses: S. vulgaris
-Sequelae: Ruptured Chordae tendinae, infarcts in GI horses S. vulgaris.
Myxomatous Valvular degeneration (Valvular Endocarditis)
-Most common cardiovascular disease in dogs, and most common cause of congestive heart failure in old dogs.
-It is age related cardiac disease of middle-age to old dogs
-Small toy breeds and medium size breeds.
-Dachshunds, Cavalier King charles spaniels with >50% prevalence by 4 years old.
-The cusps of the mitral valve are thickened by white, smooth nodules. Smooth and shiny endocardial surface of the valve and nodules. The pink staining of the valve is caused by postmortem imbibition of hemoglobin.
-Type 1: few small discrete nodules, diffuse opacity in the proximal portion of the valve
-Type 2: larger nodules evident in the area of contact, tend to coalesce with others
-Type 3: large nodules, coalesced into irregular plaque-like deformities and “ballooning” of the valve cusps, and the chord tendinea are thickened proximally.
-Lead to atrial dilation, “ jet lesions” rough, raised firm streak of endocardial fibrosis.
-Frequent accompanying myocardial alteration include arteriosclerosis, myocardial necrosis and fibrosis.
Valvular Hematocysts, valvular Lymphocytes
-Not inflammatory
-AV valves of many species: common in postnatal ruminants
-May regress, do car usually produce functional abnormalities.
-Blood-filled cysts or lymphocyte lymph-filled cysts.
- Diagnose disease of blood vessels pertaining to generalized vascular degenerative disorders.
- Diagnose inflammatory and non-inflammatory diseases of lymphatic, arterial, venous vessels. Identify diseases specific to species.
Generalized Vascular Degeneration
-Necrosis of endothelium exposes sub endothelial collagen and elicits thrombus formation.
Arteriosclerosis
-Intimal fibrosis of large elastic arteries.
-Age related
-“hardening of the arteries”
-Rarely causes clinical signs.
-The disease develops as chronic degenerative and proliferative responses in the arterial wall and results is loss of elasticity.
-Abdominal aorta most frequently affected, but other elastic arteries of arterial branches.
-Slightly raised, firm, white plaques.
Atherosclerosis
-Intimal and medial lipid deposits in elastic and muscular arteries (foam cells)
-Infrequently in animals, mostly in humans
-Accumulation of deposits (atheroma), lipid, calcium, fibrous tissue in vessel walls.
-Luminal narrowing
-Experimentally fed high cholesterol diets to pigs, rabbits, and chicken. Cattle, goats, dogs, and rats are resistant.
-Occurs in aged parrots and in dogs with hypothyroidism and diabetes mellitus, hypercholesterolemia.
-Arteries of the hear, kidney, mesentery, are prominently thickened, firm and yellow-white.
Arterial medial calcification
-Frequent lesion in animals with endocardial mineralization and involves both elastic and muscular arteries.
-Causes: carcinogenic plant toxins, vitamin D toxicosis, renal insufficiency,
-Spontaneously in horses, rabbits, aged guinea pigs, and rats with chronic kidney disease.
-Appear as solid, dense, pipeline structures with raised, white, solid intimal plaques, basophilic granular mineral deposits in elastic arteries.
Valvular Hematocysts, valvular Lymphocytes
-Not inflammatory
-AV valves of many species: common in postnatal ruminants
-May regress, do car usually produce functional abnormalities.
-Blood-filled cysts or lymphocyte lymph-filled cysts.
Cardiomyopathies
Hypertrophic
Dilated
Hypertrophic Cardiomyopathy (Think cats)
-Most common primary feline myocardial dz
-Male cats 1-3 years old
-Heritable: Main coon, Ragdoll, American shorthairs
-Less common: large breed male dogs. Symmetical hypertrophy (i.e., both left ventricular free wall and IVS) in most dogs
-Sarcomeric dysfunction: myocytes hypertrophy, and disarray (cardiomyocytes oriented perpendicular/obliquely to each other forming a pinwheel configurations). Wall thickens, lumen narrows, left ventricle’s failure to relax (diatolic failure) = left atrium enlargement, chronic heart failure +/- pulmonary edema and or pleural effusion.
-Subset of cases: IVS hypertrophied, displaced papillary muscles pull chordae tendinae and valve into left ventricular outflow tract (LVOT), resulting in obstruction during systole.
**Unique kissing lesion forms in LVOT, has a diagnostic significance (seen only in this subset of cats with hypertrophic cardiomyopathy)
-10 % of cats have increased coagulopathy and develop posterior paresis from concurrent thromboembolism of the caudal abdominal aorta = “saddle thrombus”
Arterial Thrombloembolism
-Most common cause is cardiomyopathy
-Saddle thrombus: first formed in the stagnant blood flow of the enlarged left atrium and is subsequently launched into the aorta. Also sepsis, DIC and HCM
Dilated (congestive) Cardiomyopathy. DCM
Grain free diets and DCM association?
-DCM is an important cause of congestive heart failure in cats, dogs, cattle.
-Affected dogs are often males of large breeds.
-Inherited autosomal recessive mode.
-congested heart failure of rounded hearts because of biventricular dilation.
-Biventricular or Eccentric hypertrophy, the ratio between ventricular wall and chamber diameter is decreased.
-Pulmonary edema, plueral effusion, ascites, chronic passive hepatic congestion.
-Left or bilateral CHF
-Thickened opaque endocardium, expanded atrioventricular rings, and atrial thrombosis.
-Mucus associated with it.
Secondary DCM
-Toxin: doxorubicin, irradiation, ethanol, cobalt, lead, catecholamines, histamine, and methylxanthines
-Infectious: canine parvovirus
-Nutritional: Taurine and carnitine deficiency
-Idiopathic: rare in felines. Complex genetic inheritance. Systolic heart failure rather than diastolic as seen in cats with HCM
-Rarely feline panleukopenia virus
Myocardial Diseases
Causes of Right ventricular Hypertrophy
-Dirofilariasis in dogs
-Congenital pulmonic stenosis
-Brisket disease (cattle)
-Heaves (horses)
-Chronic respiratory problems
Causes of Left ventricular Hypertrophy
-Subaortic stenosis
-Systemic hypertension
-Heart and kidney go hand in hand, one fails the other follows
- Diagnose and describe the pathophysiology of transudates and exudates within the thoracic cavity and pericardium.
- Diagnose and describe the pathophysiology of transudates and exudates within the thoracic cavity and pericardium.
