Exam 2 Flashcards

Question

Ultrasound

Answer 1

-Does not tell you anything about function but it tell us about architecture, explain to client -Widely used and valuable -Limited sensitivity and specificity for hepatic disease -Abdominal effusion enhances ultrasound images, but bone and gas densities block with acoustic shadowing

Answer 2

-Used to image a variety of hepatic disease and masses -Most commonly indicated in imaging PSS or better defined masses and vascular as pre surgical planning -Provides excellent anatomic detail particularly with 3D renditions

Answer 3

Scintigraphy -Utilization of radioactive isotopes that are taken up by tissues -Technetium-99m -Gamma camera -Animal isolated for 24-48 hours until radioactivity has decreased to background levels

Answer 4

Cytology: cells on a slide Biopsy: tissue architecture -In most cases of primary liver disease, liver biopsy is needed to establish a definitive diagnosis, prognosis and a basis for treatment -Therapy without biopsy is non specific and may actually do more harm than good -Strongly recommended before committing to the use of steroid, copper-chelating and antifibronic therapies Reasons for cytology/biopsy 1. Explain abnormal tests, especially those persisting for more than a moth 2. Explain hepatomegaly 3. Determine hepatic involvement in systemic disease 4. Stage neoplastic disease 5. Objectively assess response to treatment 6. Evaluate progression of disease

Answer 5

Advantages -Minimizes trauma and risk for patient -Least invasive -Useful for diagnosing hepatic lipidosis in cats and suspected lymphoma Disadvantages -Low diagnostic yield -Potentially misleading results -Low correlation diagnosis of liver disease

Answer 6

Cats -Higher prevalence of heapatobilirary disease -Concurrent biliary tract disease, pancreatitis, IBD "Triad disease" -Clinically serious hepatic lipidosis more common **Relatively deficient in gluconoryl transferase** -Reduced ability to metabolize drugs or toxins -Cats are more discerning in consuming food, less likely to scavenge toxins -Do not produce steroid-induced isoenzyme of SAP -SAP half-life is short in cats (6 hours) -HAC (Cushing's disease) is rare in cats -Obligate carnivores: post prandial gluconeogenesis -High dietary requirement for Arginine and Taurine (essential) Dogs -Chornic parenchymal disease is more common (fibrosis, cirrhosis, portal hypertension) -Biliary tract disease occurs but is uncommon -Secondary hepatic lipidosis is generally not clinically important -No deficiency of hepatic enzymes, but some breeds variation -Dogs are more likely to scavenge, exposing them to more potential hepatotoxins -Produce steroid-induced isoenzyme of SAP -SAP half-life is long, 66 hours - 74 hours induced -HAC is common -Adapted to use starch dietary post prandial release of insulin results in glucose storage -Lower requirement for Arginine -No obligate carnivores, no dietary requirement for Taurine, though some breeds predisposed to Taurine deficiency cardiomyopathy

Answer 7

1. Pre hepatic = hemolysis (anemia) 2. Intra-hepatic 3. Post hepatic = bile duct/gall bladder/duodenum

Answer 8

1. Hepatic lipidosis 2. Cholangitis/cholangiohepatitis 3. FIP 4. Lymphoma

Answer 9

CATS Case CBC -Mild mature neutrophilia -Rare Heinz bodies (oxidative stress) Chemistry profile -ALP elevated -ALT, GGT, Cholesterol may be normal -BUN, Creatinine and serum Bilirubin may be normal Urinalysis -Bilirubinuria -SG concentrated, pH6.5, Inactive sediment Ultrasound -Large hyper echoic liver -Falciform ligament fatty - noticeable Tx **Always vitamin K** -Impaired bile flow, impaired vitK from helpful bacteria production -IV fluids: Normosol R + KCl + VitB -Dolasetron PRN for nausea -Next day: liver FNA ultrasound guided after coagulation panel performed and WNL Dx -80% hepatocytes filled with vacuoles = lipid accumulation -Hepatic lipidosis Primary Hepatic Lipidosis -Middle aged and older cats -Massive accumulation of fat in hepatocytes -Can be reversible if treated early Secondary -May occur secondary to any disease leading to anorexia -Seen most often with pancreatitis, diabetes mellitus, IBD, and other hepatic disorders -Pathogenesis is the same as primary HL Pathogenesis -Mobilization of peripheral lipids to the liver -Deficiency of dietary proteins and nutrients important to fat metabolism and mobilization **Methionine, Arginine, Taurine** -Concurrent inappetence or anorexia: caused by stress in cat with obesity = metabolic abnormalities

Answer 10

Principles of HL Tx -Restore fluid deficits and correct electrolytes -Initiate nutritional support promptly -Treat underlying disease concurrently -Treat HE to control C/S IV fluid -0.9% saline (avoid lactate) -K supplement -NO dextrose (reduces beta oxidation of intrahepatic fats) -Add water-soluble vitamins B Nutrition -Feeding tube -High protein diet -Start gradually 20-50% RER on day 1, then increase over several days Control Nausea/vomiting -Maropitant, ondansetron or metoclopramide -Adding SAM-e and Vitamin E helps HE control -Lactulose, amoxicillin, or low dose metronidazole -Prebiotics and probiotic may help acidify the colon promoting the proliferation of non-ammoniagenic bacteria -Vitamin K SC or IM q12 hrs x3d Ursodiol -Synthetic hydrophilic bile acid (promotes choloresis = bile flow healthy bile formation) -Choleretic, anti-inflammatory, anti-fibrotic, cytoprotective, antioxidant -No available date in humans to demonstrate efficacy though Carnitine Supplement -Higher survival rate Prognosis -55-80% survival rate in intensively fed cats -Mortality high without supportive feeding -Success with secondary HL depends on primary disease

Answer 11

**Biliary disease is the second most common liver disorder in cats in the US** -Often concurrent pancreatitis, and or intestinal disease -Cholangitis: inflammation of the biliary tract -Cholangiohepatitis: inflammation of the binary tract that extends to the hepatic parenchyma

Answer 12

-Any age -Insidious history -Vague signs -Neutrophilic cholangitis: primary bacterial infection -Lymphocytic cholantitis: Primary cholangitis Neutrophilic (suppurative) cholangitis Pathogenetis -Ascending bacterial cause originating in the SI -E. coli; Streptococcus spp, Clostridium spp, occasionally Salmonella spp. -Results in neutrophilic infiltration of the bile duct lumen and walls, along with edema and neutrophils within the portal areas C/S -Acute -Most often seen in dogs young, and middle aged cats -Biliary stasis, septic, fever, jaundice, lethargy, vomiting, weight loss Dx -Findings are neither sensitive nor specific for the disease -Most have variable elevations (mild to severe) of bilirubin, ALT/AST, SAP, GGT and neutrophilia **Acurate diagnosis requires cytology, biopsy** Laparoscopic, laparotomy -Ultrasound: risk of leakage; general anesthesia strongly recommended to prevent patient movement and gallbladder laceration Tx -Based on cytology and culture/sensitivity ideally -4-6 weeks -Amoxicillin or amoxicillin/clavulanic acid -Ursodeoxycholic acid (URSODIOL) may be given as a choleric and anti inflammatory agent -Septic or very ill cat: hospitalization, IV fluids, antibiotics, and feeding support -Critical to ensure feeding to prevent secondary hepatic lipidosis

Answer 13

Pathogenesis -May overlap with chronic neutrophilic cholangitis -Slowly progressive -Infiltration of hepatic portal areas with small lymphocytes, occasionally plasma cells and eosinophils -Lymphocyte inflitrate is primarily T-cells with portal B cell aggregates -No acute signs like fever **May be difficult to distinguish from lymphoma** -Bile inflammatory infiltration is common -Inciting cause is unknown, mediates? infectious? C/S -Young to middle aged cats, Persians -Older cats -Long history (months to years) of low grade illness that comes and goes **Weight loss, intermittent anorexia, lethargy** -Jaundice if often observed -Less likely to be febrile Clinicopahtologic abnormalities -Values may be normal -Mild to moderate increases: ALT/AST, SAP, GGT -Less likely to have peripheral neutrophilia than cats with acute neutrophilic cholangitis Dx -Radiographs non-specific, may include hepatomegaly and effusion -Ultrasound can aid in identifying dilation of the biliary tree -Primary ultrasound differential is extra hepatic bile duct obstruction (EBDO) Dx -Biopsy needed for definitive diagnosis -PT/PTT testing and VitK therapy should be done prior to biopsy -PCR for antigen receptor rearrangement (PARR) assay may help distinguish lymphoma from inflammatory disease -May consider testing for Bartonella via serology or PCR General Tx -Look for underlying disease and manage it -EHBDO, choleliths, trematodes, IBD, pancreatitis -Antimicrobials: empiric coverage gram (-) and anaerobes -Tx neutrophilic: several months -Tx non-neutrophilic until biopsies return & based on C/S **Ursodeoxyxholic acid: cytoprotectivem antifibrotic, choleric, antioxidant** -Maintain adequate nutrition -Supplement water soluble vitamins B12 deficiency -Vitamin K if jaundice -Fluid therapy -Maintain normal serum potassium -Antioxidant therapy -Vitamin E -SAMe

Answer 14

-Differing opinions -Often immunosuppressive corticosteroids but may not lead to resolution/cure -URSODIOL recommended -SAMe and VitE recommended -Very ill cats require hospitalization, IV fluids, medical feeding support -Critical to ensure feeding, prevention of hepatic lipidosis -Concurrently treat associated disease such as IBD or pancreatitis

Answer 15

-Disorder commonly spontaneously cycles -Some cats have very long remission or cure with chronic medical management like IBD -No long-term prospective studies on the efficacy of treatment -Death -Cirrhosis -Biliary cirrhosis -Progression to lymphoma -Underlying or associated conditions (IBD, pancreas) **Get biopsy from the beginning, long-term rechecks, variety of drugs for management**

Answer 16

-Primary liver tumors more common in dogs than cats **1-3 % of all neoplasia in cats, but up to 7% of the non-hematopoietic tumors** -Benign liver tumors are more common in cats than dogs -Most common in older cats 10-12 yrs of age

Answer 17

C/S -Lethargy -Vomiting -Weight loss -Ascites -Jaundice -Hepatomegaly or liver mass on abdominal palpation **50% or > of cats with liver tumors may be asymptomatic** Dx -Elevated liver enzymes, bile acids, mild anemia, neutrophilia are common but non-specific Primary Tumors -Bile ducts adenomas >50% in cats -Bile ducts carcinomas (most common malignant hepatic tumor in cats) -Hepatocellular adenomas more common than adenocarcinomas in cats -Hemangiosarcomas is uncommon, but is the most likely primary hepatic sarcoma in cats Secondary tumors -Lymphomas most common -Leukemias -Histicytic tumors -Mast cell tumors -Metastatic tumors (ie, hemangiosarcoma, which may be a primary or secondary metastasis) Dx -Histopathology key -FNA for suspected lymphoma Tx -Dependent on the type of tumor -Generally good outcome if it can be excised and is benign, guarded if malignant -Lymphoma can respond well to chemotherapy

Answer 18

-More common in dogs than cats -Congenital more common than acquired -Congenital: extra hepatic or intrahepatic, single (most commonly) or double vessels -Purebred cats are overrepresented C/S -GI: intermittent diarrhea, vomiting -Urinary: Cystitis associated with rate stones -PU/PD -Neurologic: signs of HE -Poor or stunted growth -Copper colored irises Dx -History and C/S -Elevated pre and post prandial bile acids -Radiographs 50% show small livers -Clinpath: Low BUN, mild increased liver enzymes and microcytosis -Visualization of the shunt or imaging, ultrasound, CT angiography, or portal venography Tx -Complete or partial ligation of the shunt -Cats need more than medical management due to higher obligate protein metabolism = production of > ammonia than dogs Prognosis -Good if it can be ligated -Post operative mortality higher in cats than dogs

Answer 19

-Hepatic injury due to exposure to environmental toxins -Cats have limited capacity for glucocoronidation, more sensitive than dogs to drugs and compounds **Diazepam, Methimazole, Acetaminophen** Picky eaters, less likely than dogs to experience hepatic toxicosis

Answer 20

1. Hyperthyroidism: affected cats frequently have elevated liver enzymes >75% have SAP 2-12 x higher than normal >50% .. ALT/AST 2-10 x ... >90% .. at least one values elevated 3% are hyperbilirubinemic

Answer 21

-Inflammation of the pancreas, duodenum, and or biliary tree is common in cats and is known as "Triad disease" -Pancreatitis can lead to bile duct obstruction EBDO leading to severe cholestatic hepatopathy

Answer 22

-Hepatomegaly associated with mild to moderate lipid deposits is common finding in diabetic cats -Mild to moderate increases in liver enzymes are commonly noted in diabetic cats -Associated with secondary hepatic lipidosis

Answer 23

Hepatobiliary Diseases in the Dog 1&2 1. Chronic hepatitis a. Idiopathic b. Copper storage c. Infectious 2. Acute hepatitis a. Infectious b. Toxic 3. Cholangitis 4. Cholecystitis 5. Gallbladder mucocele 6. EBDO 7. Congenital PSS 8. Acquired PSS

Answer 24

-Characterized by hepatocellular necrosis and death, with variable inflammatory cellular infliltrate -Results in regeneration, fibrosis, and cirrhosis in the end stages -Elevated liver enzymes > 4months **Syndrome with many causes, which lead to Chronic inflammation, apoptosis and/or necrosis, regeneration** -LOW ALBUMIN, LOW BUN, LOW GLUCOSE, LOW CHOLESTEROL -High bilibirubin, Ascites, HF, coagulopathy -Cirrhosis: diffuse, bridging fibrosis, and regenerative nodules -Portal hypertension and numerous portosystemic collateral shunts are common sequelae -Liver failure clinical presentation: Hyperbilirubinemia, coagulopathies, ascites, and or HE - Cause usually unknown **Leptospirosis, CAV-1, Bartonella, Leishmania, Mycobacterium, Histoplasmosis, Helicobacter** -Drugs, toxins, Immune-mediated, Idiopathic **C/S absent until disease is advanced** **Recognize key signs in advance warranting additional testing and intervention early** **Don't just watch the elevated liver enzymes** Breed, gender and age matter -Bedlington terrier -Doberman pinscher FEMALES -Sky terrier -West highland white terrier -English springer spaniel FEMALES -Labrador retriever FEMALES -Golden retriever -Dalmation FEMALES -Crocker spaniels MALES -Jack russell terriers -German shepherds -Beagle -Standard poodle -German pointer -Great dane **Middle-aged to older dogs**

Answer 25

Pathogenesis -Unidentified causes may include: viral, bacterial, prior toxic event, immune-mediated -Hepatocyte swelling and subsequent fibrosis result in loss of functional hepatic mass -End stage disease is characterized by cirrhosis and portal hypertension Idiopathic -Chronic portal hypertension -Acquired portosystemic shunting that acts ad "pressure relief" valves -End-stage hepatic triad: **Ascites, gastrointestinal ulceration, hepatic encephalopathy** C/S -Inappetence -Anorexia -Malnutrition -Negative nitrogen balance -Coagulopathies -Cirrhosis **75-85% function loss first** -Treatment less successful at this point -Signs may be low grade, intermittent and non-specific -Common signs: vomiting, diarrhea, anorexia, PU/PD **Thin body condition scores** -Abdominal pain due to inflammation or GI ulceration -Late stage ascites, jaundice. Clinicopathologic abnormalities -Liver package: Elevated ALT/AST, SAP, GGT, bilirubin, bile acids, ammonia; decreased BUN & Albumin **Chronically elevated ALT is the most consistent finding, but non-specific** Investigate more -Hepatocellular enzymes can normalize at end stage = fibrosis Dx -Suspicion based on signalment, c/s, presentation, bloodwork values -Radiographs: normal to small liver, ascites will obscure details -Ultrasound: small, diffuse hyperechoic parenchyma, nodules may be present but can not differentiate benign from malignant process on appearance **Biopsy full thickness is key** -Histology necessary for definitive diagnosis -Need multiple samples from different lobes, edges and middle pieces 12-15 portal triads -Recommend laparoscopy or surgical laparotomy -Qualitative and quantitative copper analysis -Cultures (aerobic/anaerobic) -Special stain and or immunohistochemistry may be needed Treatment -Remove the underlying cause: Copper reduction or dietary restriction. Antibiotics if suspected or confirmed hepatic or concurrent infection. Avoid: tetracyclines, potentiated sulfonamides, nitrofurantoin, and erythromycin = hepatotoxic -Decrease immune response and inflammation: glucocorticoids should be based on biopsy results. Anti-inflammatory doses prednisone/prednisolone are most commonly used to decrease fibrosis. Immunosuppresive should not be used chronically. Consider dexamethosone, methylprednisone if ascites present. Azathioprine, Cyclosporine, Mycophenolate -Slow/prevent fibrosis: anti-fibrotic Colchicine -Provide antioxidant and hepatosupportive therapy: Ursodeoxycholic adic (increases bile flow, immunomodularoty, reduces inflammation). Vitamin E, SAMe (S-adenosylmethionine), Glutathione precursor. Silybin (milk thistle extract) Elemental Zinc: antifibrotic, anti-inflammatory, decreases gut absorption of copper, monitor blood levels periodically. -Prevent complications or liver disease: treat HE, Ascites and coagulopathy Antiacids -Famotidine, ranitidine, ameprazole Antiemitics -Ondansetron, metoclopramide, maropitant Diuretics for Ascites -Spironolactone first choice -Furosemide can be added if needed Supportive therapy -Nutrition: protein nor restricted unless HE present -Feed moderate amount of high quality protein -Low copper diet PRN Monitor -C/S -PE findings -Trend and CHEM profile -ALP will increase with glucocorticoid therapy -Repeat liver biopsy 6-12 mts after initial therapy Prognosis -Varies -No cure -Quality if life can be improved

Answer 26

Pathogenesis -Copper is normally excreted in the bile -Can accumulate in an hepatic disease involving cholestasis -Zone 1 cells (periportal) storage usually -Amount stored is not correlated to the severity of disease **True copper storage disease represents a genetic defect in transport and or storage** -Bedlington Terrier: marked zone 3 cells accumulation (centrilobular) -Other breeds affected: labrador retriever, doberman pinscher, dalmatians, skye terriers, west highland terriers. C/S -Depend on breed and acute vs. chronic state -Rapid build up can result in fulminant hepatic necrosis and hemolytic anemia due to rapid copper release in the blood stream -Slow accumulation can take several years, chronic hepatitis Clinicopathologic abnormalities -Persistently elevated ALT -Similar values as seen in chronic hepatitis Dx -Liver biopsy with special staining -Genetic testing for COMMD1 gene Tx -Hospitalization for supportive care may be needed if fulminate hepatic failure -IV fluids: avoid lactate or acetate -Dextrose in saline with supplemental potassium a good initial choice -Supplement vitamins B, K for prolonged PT, PTT, PIVKA -Control GI bleeding: antiacids, fresh frozen plasma if needed **Copper chelation, followed by zinc** -D-penicillamine: takes months to chelate but the drug profile is best known for dogs -Trientine: rapid removal of copper, expensive -Continue chelation until normal blood values of liver enzymatic/biopsy -Vitamin E and SAMe -Once copper levels are normal maintain in liver diet and zinc oral supplement

Answer 27

Pathogenesis -Uncommon -Unknown organisms -CAV-1 has been implicated -Possible Helicobacter, atypical Leptospirosis -Bartonella henselae implicated Tx -Management of chronic disease secondary effects, as discussed for chronic hepatitis -Treat any identified underlying infectious agents

Answer 28

-Less common in dogs -Prognosis for acute fulminate failure in the dog is guarded to grave prognosis -Inciting causes can be infectious, toxic, drug induced, metabolic, or associated with heat injury Pathogenesis -Similar to chronic infectious hepatitis, CAV-1 and leptospira bacteria are the most important infectious organism -Acetaminophen, phenobarbitol, carprofen, xylitol and aflatoxin C/S -Related to significant loss of functional hepatic mass -Also related to the massive release of inflammatory cytokine and tissue factors as a result of hepatocyte necrosis and death -Vomiting, anorexia, dehydration, polydipsia, fever, abdominal pain -HE, jaundice, evidence of bleeding disorder (petechia, melena, hematemesis); ascites, splenomegaly due to portal hypertension -Renal failure possible Clinicopathologic abnormalities -ALT/AST marked elevation >100 fold increase -Jaundice SAP elevation -Hypoglycemia and hypokalemia are common -Prolonged PT, PTT and thrombocytopenia are associated with DIC Dx -Based largely on hystory, c/s, and blood work -Diagnostic imaging may not be useful since changes are peracute/acute and not often visible Tx -Prognosis guarded to poor for fulminating failure -If dog makes it through acute phase there is a good change of complete recovery -Intense supportive care is required, ICU BEST

Answer 29

-Less common in dogs than cats -Cholangitis -Cholecystitis -Gallbladder mucocele -Extrahepatic bile duct obstruction EBDO

Answer 30

Pathogenesis -Similar to neutrophilic cholangitis in cats -No breed, age or sex predilection -Typical signs include: vomiting, anorexia, and jaundice +/- fever -Can be associated with history of pancreatitis or gastroenteritis, suggesting an ascending infection similar to cats Dx -Based on history, c/s and blood work -Ultrasound imaging useful to rule out bile duct obstruction and gallbladder mucocele -Culture of bile and liver biopsies are important to establish a diagnosis **Enteric organisms are most common: E. coli, Enterococcous, Klebsiella, Clostridium spp. ** Tx -Extended antibiotic therapy based on culture and sensitivity -Supportive care and/or hospitalization as needed for hepatic failure Prognosis -Good with appropriate antibiotic therapy

Answer 31

**Common cause of biliary tract disease in dogs** -Middle-aged to older dogs -Proposed that sterile or septic inflammation of the gallbladder walls predisposes to mucocele -Genetic mutation recently discovered -ALP, GGT, cholestatic pattern C/S -Vary -Similar to other hepatobiliary disease -Gallbladder rupture and peritonitis can occur Tx -Generally surgical -Perioperative mortality is high -Medical management: low fat diet, choleretic URSODIOL, antioxidant SAMe

Answer 32

Causes -Inflammation of the pancreas, duodenum or biliary tree -Neoplasia **Complete blockage = alcoholic feces, absent urobilinogen and Vit K deficiency coagulopathy** not compatible with life

Answer 33

Congenital PSS -Most common -Extrahepatic shunts are most common in small breeds: Cairn terrier, Yorkshire, Terriers, Westies, Maltese, Miniature Schnauzers. -Intrahepatic shunts are usually seen in large breed dogs -Cryptoschidism in 50% of males Clinicopathologic abnormalities and Dx -Bile acids can be used to screen suspect puppies prior to placement in homes but some false positives can occur -Vascular disorders in young dogs such as hypoplasia of extrahepatic portal vein and intrahepatic microvascular dysplasia -Affects primarily small breed dogs (Yorkies and Cairns) -Characterized by non-cirrhotic portal hypertension Tx -Surgical ligation of the anomalous vessel is generally recommended -Partial occlusion is initially recommended to prevent chances of post operative portal hypertension, which could lead to multiple acquired shunts **Ameroid Constrictor Ring** -Medical management important for several weeks post op -Dietary management -Moderate protein diet -Antibiotics -Soluble dietary fiber helps manage and prevent HE -High pressure PSS dogs Prognosis -Good for survival, normal after surgery and post op medical management

Answer 34

1. Abscess 2. Nodular hyperplasia 3. Neoplasia

Answer 35

Pathogenesis -Hematogenous spread via septic embolism to liver parenchyma -Puppies: often umbilical vein inflammation -Adults: inflammatory disease of pancreas or hepatobiliary system Clinicopathologic abnormalities -Depends on extent of liver involvement -Elevated enzyems, neutrophilia with bands and left shift C/S -Lethargy -Anorexia -Vomiting -Fever -Dehydration -Abdominal pain -Variable: hepatomegaly Dx -Presenting signs -Bloodwork -Ultrasound -CT -FNA can help distinguish from a mass -Culture and sensitivity of aspirate material -Gram (-) organisms most frequently isolated -Staph and Clostridium Tx -Surgical excision of abscess -Antibiotics gram (-) and anaerobes 6-8 weeks -Supportive care -Resolution of underlying disease -Ultrasound guided drainage if surgical removal is not an option + long-term antibiotic therapy

Answer 36

Pathogenesis -Benign condition of older dogs -70-100% of dogs >14 yo -Macronodular masses 2-5 cm -Micronodular masses identified on biopsy -Adjacent parenchyma is compressed by growth of the nodule which can result in localized cholestasis and generally mild increase in hepatic enzymes -Tissue biopsies are the standard diagnostic tool -FNA not sensitive enough to distinguish from neoplasia

Answer 37

-Primary hepatic tumors are uncommon in dogs -Malignant tumors are more common in dogs than cats -Metastatic are 2.5 more common than primary hepatic tumors Hepatocellular carcinoma -Most common primary liver tumor -Metastasizes frequently Hepatocellular adenomas -Uncommon in dogs Biliary carcinoma -Second most common primary liver tumor in dogs -Aggressive and metastasizes Primary sarcomas -Hemangiosarcomas -Leiomyosarcoma: uncommon, locally aggressive, high metastatic Tx -Surgical excision of solitary mass curative -Poorly responsive to chemotherapy Exception: dog with hepatic envolvement of systemic lymphoma; can have excellent response to chemotherapy (primary hepatic lymphoma has poor response rate)

Answer 38

**Ammonia NH3 is the most important cause of HE** -Lipophilic and highly lipid soluble passes freely across cell membranes -Ammonium NH4, is not lipid soluble and must be transported across cell membranes

Answer 39

Pathophysiology -Increased Blood Ammonia Medical management -Goal is to restore neurological function 1. Decrease the formation of encephalotoxins (both GI derived and peripherally derived) 2. Eliminate/control factors that precipitate HE 3. Correct acid-base and electrolyte abnormalities -Lactulose: promotes osmotic diarrhea. Can be administered as an enema for acute HE -Antibiotics: Amoxicillin and metronidazole. Low dosages to avoid neurotoxic side effect -Identify and treat concurrent infections and inflammation Dietary considerations Dogs -Avoid prolonged fasting or excessive protein restriction to prevent catabolism -Feed smaller, more frequent amounts -Feed fat in normal amounts, do not restrict unless GI disturbances (e.g., steatorrhea) -Avoid very high fat diets 1. High digestible fiber 2.Adequate protein 4 g/100 kcal per day 3. Carbohydrates available 4. Vitamins and minerals: restrict manganese and copper 5. Highly palatable 6. Zinc for urea cycle and muscle metabolism of ammonia 7. Arginine for cats 8. Small frequent meals -Dairy: low in arginine -Egg: high in methionine: converted to mercaptans by GI bacteria -Fish: high in purines, can increase uric acid production Commercial prescription diets -Hill's I/D -Purina HP -Royal canine hepatic diet -Supplemented with EFAs, antioxidants and restricted copper levels Other -Probiotics: fortiflora, nutramax, etc -Prebiotics: fiber supplementation -Zinc acetate -Ornithine aspartate: promotes conversion of NH3 to urea Control precipitating factors -High protein meal -Large meal = increased glutamine -GI bleeding -Constipation = increased bacterial contact time with substrates in colon -Azotemia -Catabolic metabolism -Poor quality protein -Blood transfusion -Metabolic alkalosis -Hypokalemia -Sedatives/anesthetics -Estrus -Inflammation

Answer 40

-Emergency -Treat/remove precipitating factors -NPO 24-48 hrs -Fluid therapy: avoid lactate/acetate -Treat/monitor for hypoglycemia -Treat/monitor hypokalemia -Hypo/hyperthermia -Admin enemas to remove ammonia from colon -Instill neomycin in colon -Ampicillin IV -Treat seizures: Propofol bolus, CRI, phenobarbital, Levetiracetum (Keppra), Diazepam limited efficacy and not tolerated sometimes. Diagnosis -Look for evidence of hepatic disease -CBC microcytosis, poikliocytosis -Chem: ALT/AST, cholestatic GGT/ALP, BUN, glucose, cholesterol, albumin, increased bilirubin -UA: ammonium bitrate or bilirubin crystals -Bile acids elevated -Coagulation test -Radiographs -Ultrasound -Scintigraphy: confirm PSS -Whole blood manganese elevated -MRI/CT cerebral edema ** do not treat until hemodynamically stable** Mannitol, hypertonic saline, elevation of head -Benzodiazepine antagonist if stupor comma - Flumazenil -Anticonvulsants: Levetiracetam, Potassium bromide, Phenobarbital, Propofol, benzodiazepines. -Enemas, antibiotics, lactulose PO, Polyethylene glycol 3350.

Answer 41

-Occurs most commonly in dogs with chronic liver disease -Uncommon in cats -Leads to: Intestinal wall edema, ulceration, ascites. Acquired PSS to help limit increase in pressure in portal system

Answer 42

-Catastrophic GI or esophageal ulceration is likely most common cause of death in dogs with chronic liver disease -Proximal duodenum most common site -Prevention of GI ulceration is crucial since treatment is not always successful -Avoids NSAIDs, corticosteroids -Control triggers: sepsis, protein-calorie malnutrition (leading to glutamine deficiency at enterocyte level) -Enterocytes need glutamine to heal -Avoid hypotension, hypovolemia -Enteral feeding is crucial in period of anorexia -Antiacid questional bc site of ulcers is duodenum -H2 blockers or PPIs should be used if active ulcer or melena are present -Carafate (sulcralfate) most effective -Control coagulopathies: vit K +/- plasma transfusions

Answer 43

-Transudate or modified transudate -Primary mechanism for formation of ascites is portal hypertension -RAAS -Hypoalbuminemia Tx -Spironolactone most effective as it blocks aldosterone -Moderate sodium restriction -NO Loop diuretics: furosemide NO -Abdominocentesis if respiratory compromise

Answer 44

Exocrine pancreatic disease

Answer 45

Acinar: secrete digestive enzymes, aqueous NaCHO3 90% Endocrine: Hormones, insulin, glucagon. 10% Intrinsic factor: health of the intestinal cells. Vitamin B12 needed by ileum, when enteropathy present = deficiency in Vitamin B12 possible. Cats get it more than dogs, triaditis

Answer 46

Cats -Pancreatic duct joins bile duct to form a common outflow tract to the duodenum -IF secreted solely by pancreas -Commonly a part of the "triad" disease: cholangiohepatitis, SI disease, pancreatitis. -Most cases low grade chronic interstitial disease Dogs -2 pancreatic ducts -Pancreas produces majority of IF, but small percentage comes from stomach -Pancreatitis and endocrine disease association -Most cases are acute -Greater recognition of chronic, low-grade disease

Answer 47

-Inappropriate early activation of trypsinogen in the pancreas as a result of increased autoactivation of trypsinogen -Reduced autolysis of prematurely activated trypsin (enzyme that aids in digestion) -Pancreatic auto digestion -Surrounding fat necrosis -Focal to generalized peritonitis -Systemic inflammatory response, even in mild cases -Possible multiorgan failure in severe cases -Disseminated intravascular coagulation

Answer 48

-Terrier -Miniature Schnauzers -Domestic short hair cats Underrepresented -Large, giant breeds -Labrador and Husky affected -Any breed or cross-breed can be affected

Answer 49

Increased values -BUN, creatinine -ALT, AST, SAP, GGT, bilirubin -Neutrophils, bands, left shift Decreased values -Potassium, chloride, platelets Variable -Sodium, calcium, phosphate, albumin, hematocrit

Answer 50

-Based on clfinicopathologic criteria -Hepatic: elevated liver enzymes >3x upper normal range -Renal: elevated BUN, Creatinine -Leukocytes: >10% bands or WBC >24 x 10^3/uL -Blood glucose elevated (endocrine pancreas) -Abnormal bicarbonate or anion gap = acid-base imbalance

Answer 51

Dogs -Hx of high fat meal recently -Cushing's, diabetes mellitus, or hypothyroidism concurrent -Hx of seizure drugs or chemotherapy -Vary with severity of disease -Abdominal pain, anorexia, MOF and DIC -Vomiting, dehydration, collapse and shock -Primary Ddx: intestinal foreign body or obstruction Cats -Hx of concurrent cholangiohepatitis, IBD, hepatic lipidosis, or combination of these -"Triad" disease - cholangiohepatitis, IBD, and pancreatitis -Unexpectedly mild signs, even in the face of severe disease -Anorexia, vomiting, abdominal pain <50% of cases

Answer 52

Dogs -Mild, intermittent GI signs -Episodes or anorexia, vomiting, mild hematochezia, postprandial pain -Can present with acute-on-chronic pancreatitis **Chronic pancreatitis is the most common cause of EBDO** Cats -Mild non-specific signs -Most often associated with concurrent disease than acute pancreatitis: IBD, hepatic lipidosis, cholangiohepatitis, renal disease

Answer 53

-High index of suspicion based on breed, C/S and history **PLI gold standard test for pancreatitis** -Amylase, lipase: not sensitive or specific for diagnosis -RAdiographs -Ultrasound

Answer 54

-IV fluids: prevents pancreatic ischemia -Replacement fluids LRS, normosol, plasmalyte are usual choices -Correct electrolyte abnormalities, hypokalemia Analgesia **Opioids, avoid NSAIDs** -IV low dose Ketamine, good for motility but not enough for analgesia -IV lidocaine; higher levels toxic in cats Diet -Do not withhold food for extended period -Early nutrition is key, especially when severe pancreatitis -NPO contraindicated in cats, due to potential for hepatic lipidosis Enteral feeding -Jejunostomy tube -Prepyloric feeding, nasogastric or gastrostomy tubes -Low fat, high digestible diet -Parenteral nutrition if needed Antiemetics -Management of nausea to be able to feed -Maropitant first choice -Metoclopramide -Butorphanol -Phenothiazines: hypotension risk -5-HT3: Ondansetron Gastroprotectants -H2 blockers: famotidine, ** avoid cimetidine due to P450 inhibition** -PPIs: omeprazole Antibiotics **If evidence of infection is present** -Aerobic and anaerobic coverage: Enrofloxacin + metronidazole or amoxicillin -Amoxicillin/clavulanic acid Supplementation -Vitamin B12 -Intrinsic factor absorption -Assume cats are deficient since all IF comes from pancreas -Measure blood levels in affected patients -Supplement parenterally with cobalamin

Answer 55

-Results from insufficiency of pancreatic enzymes -Pancreatic acing atrophy (PAA) is most common recognized etiology in dogs -Dogs develop diabetes mellitus before or after EPI onset -Up to 70% of dogs also have SI bacterial overgrowth SIBO -Bacteria deconjugate bile salts, which adds to fatty diarrhea -Cobalamin deficiency is common -This deficiency exacerbates small intestinal dysfunction Cats -Chronic pancreatitis is the most common cause of EPI -Idiopathic reasons EPI C/S -Weight loss -Fatty diarrhea -Pancreas is the only source of Lipase -Strong voracious appetite -Ddx: maldigestion, malabsorption enteropathy, hyper metabolism, parasite burden Dx -High suspicious based on breed and history and presentation -Most often normal to mild changes on CBC and serum biochemistries -Marked changes trigger a hunt for other concurrent disease **Trypsin-like immunoreactivity TLI is the most accurate test for EPI** -Cobalamin and folate levels should be measured. SIBO or IBD, associated abnormalities with bacterial overgrowth, bacterial dysbiosis Tx -Supplementation of pancreatic enzyme powder sprinkled on food -H2 blocker helps to increase absorption bc stomach pH decreases enzyme -Dosage can be reduced long-term but it can not be stopped completely -Antibiotics: Tylosin, metronidazole may be necessary -Supplement cobalamin until levels return to normal

Answer 56

Dogs -Low fat diet but not necessary -Avoid high fats -Moderately fat restricted, highly digestible diet and reasonable caloric is best -Coconut oil for additional calories ok -Do not add MCT to the diet

Answer 57

-Uncommon in cats and dogs -Pancreatic adenocarcinomas are very aggressive, metastasized at the time of diagnosis -May be asymptomatic or only mild signs of pancreatitis -Prognosis is very poor for adenocarcinomas Pancreatic adenomas -Rare but reported in cats -Neuroendocrine tumors include insulinomas (persistent hypoglycemia) gastrinomas (GI ulcerations, esophagitis) -Nodular hyperplasia is common in dogs and cats

Exam 2 Flashcards

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