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92 Cards in this Set
- Front
- Back
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What are the 4 patterns of hepatic injury?
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1) Focal
2) Acute generalized injury 3) Chronic generalized injury 4) Anatomical or functional injury |
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What is focal liver damage? What are 3 examples?
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Small area of damage
-abscesses -neoplasia -solitary infarctions *rarely cause overt clinical signs |
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What type of zonal injury is most common in the liver?
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Centrilobular or peri-acinar
-widespread zonal injury can induce signs of insufficiency |
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What is centrilobular zonal injury of the liver?
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Cell damage around central veins
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What is peri-acinar zonal injury of the liver?
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Zones II and III of the acini affected
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What is zone 1 of the liver? What processes occur here?
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Relies heavily on oxygen
-area where urea synthesis and oxidative metabolism occur -*more damaged by hypoxia |
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What is zone II of the liver? Zone III?
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Zone 2: attributes of zone 1 and 3
Zone 3: Glycolysis and lipogenesis (*requires less O2) |
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What usually causes damage to the 3 zones of the liver?
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Zone 1: hypoxia
Zone 2 & 3: toxins |
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What are 4 general causes of acute generalized liver injury?
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1) Toxic
2) Infectious 3) Necrosis 4) Inflammation *often induces signs of hepatic failure |
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How do livers with acute generalized injury grossly appear? On histopathology?
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Grossly: Pale, enlarged and friable
Histo: inflammatory cell infiltrates in areas of cell death or surrounding portal triads |
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Compare the terms hepatitis and cholangitis.
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Hepatitis: inflammation of parenchyma
Cholangitis: inflammation of the biliary system |
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Is acute generalized hepatic injury or chronic generalized hepatic injury a superior prognosis?
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Acute generalized injury is a superior diagnosis bc animal may be able to recover
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When are clinical signs of chronic generalized hepatic injury apparent?
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> 75% parenchyma lost/ fibrotic
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When does fibrosis of the liver occur?
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When rate of cell death exceeds hepatocyte regeneration
-fibrous tracts interrupt oxygen supply to cells and increases rate of cell necrosis= self perpetuating cycle till get cirrhosis |
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What is cirrhosis?
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Widespread fibrosis, nodular regeneration and biliary hyperplasia
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What is a cause of anatomical or functional liver damage?
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Vascular shunts
-anoxic damage -failure to detoxify blood |
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******What is the most common cause of acute hepatitis and hepatic failure in horses?
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*****Theiler's disease
-idiopathic acute hepatitis |
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What is a risk factor for developing theiler's disease (idiopathic acute hepatitis)?
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Disease often develops 4-10 weeks after the tetanus anti-toxin is given
-Equine biologic (plasma or serum) in ~20% of cases -outbreaks include horses not given biologics |
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True or false. Idiopathic acute hepatitis has NOT been confirmed by testing of clinical cases or experimental transmission.
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True
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What age of horses are most commonly affected by Theiler's disease?
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Adult horses > 2 years
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What horses are at increased risk of fatal idiopathic acute hepatitis?
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Lactating mares
-1-3 months post foaling -related to routine TAT? |
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What is the clinical course of Theiler's disease (IAH)?
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Acute progressive hepatic failure over 2-7 days
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What are 4 clinical signs of the acute progressive hepatic failure due to Theiler's disease?
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1) Jaundice, anorexia, depression
2) Photosensitization -depending how long they have the disease 3) Yawning, HE (80% of cases) 4) Fever RARE *subclinical cases very likely |
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What is it about clinical signs and history that suggest idiopathic acute hepatitis?
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-Rapidly developing signs of hepatic failure
-History of TAT or other biologics |
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There will be an increase in what 4 chemistry parameters in a horse with idiopathic acute hepatitis?
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1) total bilirubin and UCB
2) Serum bile acids 3) SDH, AST, LDH 4) GGT and ALP |
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What is seen on an ultrasound of a horse with idiopathic acute hepatitis?
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-decreased parenchymal echogenicity
-Heterogenous appearance (acute necrosis) |
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What is seen on a liver biopsy of a horse with idiopathic acute hepatitis?
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Diffuse necrosis
-most severe in centrilobular and midzonal areas |
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How do the livers appear post-mortem in a horse with idiopathic acute hepatitis?
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Enlarged, pale and diffusely mottle liver
-sometimes small (massive hepatic collapse) |
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What is the treatment for idiopathic acute hepatitis in horses?
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Supportive
-IV dextrose and electrolytes to reduce hepatic energy demand and maintain plasma volume -plasma (coagulopathy) -corticosteroids controversial |
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How high is mortality from idiopathic acute hepatitis? When does death usually occur?
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Can approach 90%
-Death in 5 days or gradual recovery in 7-10 days -Recovery may be protracted and incomplete (may develop chronic liver failure) |
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How can you prevent idiopathic acute hepatitis?
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1) Avoid offending products?
2) Mention risk to owners when giving TAT -avoid routine TAT to post-foaling mares -encourage routine tetanus prophylaxis |
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Why should owners screen other horses on the property when a horse has a suspected case of idiopathic acute hepatitis?
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often affects multiple horses and can be subclinical
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What is Tyzzer's disease? What age of horses are affected?
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Acute and highly fatal bacterial hepatitis
-foals 1-6 weeks of age -probably not contagious |
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What is the causative agent of Tyzzer's disease?
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Clostridium piliformis
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What horses shed clostridium piliformis?
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Health mares that are resistant
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What are the clinical signs of Tyzzer's disease?
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Sudden death at 7-42 days old
-fever, icterus, depression, anorexia, diarrhea, seizures |
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At what time post infection is Tyzzer's disease usually most fatal? What can you do to try and save the foal?
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In 48 hours= most fatal
-attempt high dose penicillin and gentamicin -intensive support -only 1 foal ever reported to live |
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Tyzzer's disease is most commonly diagnosed upon necropsy. What are 2 things you will see upon necropsy in a foal that died from Tyzzer's disease?
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1) Multifocal hepatic necrosis
2) Intracytoplasmic bacteria -gram + rods -Fastidious and hard to culture -PCR and FAB |
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What is the common name for infectiousnecrotic hepatitis?
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'Black disease'
-sudden death of grazing animals (sheep) |
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**What is the agent that causes black disease?
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Toxemia with Clostridium novyi type B
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Where is the clostridium novyi type B organism found?
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Ubiquitous: soil, bowel, liver of grazing animals
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Clostridium novyi type B is an organism that is normally found in the liver of grazing animals, so what makes Black disease develop?
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Hepatic damage--> anaerobic --> germination, proliferation and production of 3 exotoxins
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What can cause of hepatic damage that results in clostridium germination?
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1) Migrating larvae of Faciola hepatica
-common liver fluke, only takes 1 fluke 2) Other causes: -Fascioloides magna -Dicrocoelium dendriticum -Cysticercus tenuicollis -liver biopsy |
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What is the pathogenesis of infectious necrotic hepatitis?
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-spores consumed and shed by grazing animals
-some bacteria cross the gut and disseminate into the RE system (Kuppfer cells) -hepatic damage and anaerobic environment allows spores to germinate and produce exotoxins ---> enlarging zones of coagulation necrosis & widespread systemic effects from toxemia |
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What are the clinical signs of infectious necrotic hepatitis?
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Usually sudden death
-fever, anorexia, depression, separation from herd |
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What are 4 findings of infectious necrotic hepatitis on necropsy?
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1) Carcass decomposed
-more decomposed than expect 2) Widespread SQ hemorrhage 3) Blood tinged body cavity fluids -normal urine in contrast to 'red water' 4) Swollen and congestive liver -focal coagulative necrosis -evidence of fluke migration in ruminants |
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What is a differential for the blood tinged body cavity fluids?
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*anthrax
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Other than a standard necropsy, what are some further diagnostics that can be done in an animal that has infectious necrotic hepatitis? (4)
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1) Gram stain impression smears of liver
-large gram + rods -interpret cautiously 2) Culture difficult (anaerobic) 3) FAB on impression smears 4) Specific exotoxin identification -not practical, but confirming procedure of choice |
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What treatments are available for infectious necrotic hepatitis?
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-usually not indicated
-penicillin or oxytet, supportive care -no antiserum -vaccinate other ruminants immediately -consider mass administration of long lasting antibiotics |
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What are 4 ways to prevent infectious necrotic hepatitis?
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1) Burn, bury or remove carcasses
-carcass full of clostridium 2) Reduce fluke infestation -pasture management -limit access to natural water water source and canals -appropriate antihelmintic use 3) vaccination 4) Commercial bacterin/toxoids (combination) |
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How long do the commercial bacterin/toxoids for infectious necrotic hepatitis last?
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5-6 months
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What vaccine for infectious necrotic hepatitis may be more affective in high risk herds?
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Monovalent Clostridium haemolyticum
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When should vaccinations for infectious necrotic hepatitis be given?
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Time vaccination w/ fluke season
-single annual injection in harsh climates -2 injections 5 months apart in gentler climates (longer fluke transmisson) |
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What is the common name for bacillary hemoglobinuria?
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Red water
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What are 2 infectious hepatic diseases of cattle that appear very similar?
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Black disease & red water
-both caused by clostridium, same pathophysiology -black disease= no hematuria |
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What animals are affected by bacillary hemoglobinuria?
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Sudden death in ruminants and occasionally horses
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What is the causative agent of Red Water?
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Syndrome of toxemia from Clostridium haemolyticum (clostridium novyi type D) infection
-black disease= clostridium novyi type B |
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What are the results of phospholipase, tropomyosinase and lipase produced in animals with Red water disease?
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Causes localized hepatic necrosis and IV hemolosysis
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What is the pathophysiology of bacillary hemoglobinuria?
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-bacterium exists in soil w/ spores in the feces, liver and urine of healthy animals
-anaerobic regions of hepatic tissue allow germination and toxin production (migration of larval liver flukes) |
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How does the distribution of Black disease and Red Water vary?
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Red Water is strongly regional in nature for unknown reasons, certain farms close together will have the same problem
-black disease=not regional |
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What are the clinical signs of bacillary hemoglobinuria antemortem?
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-usually sudden death
-fever, anorexia, herd separation, icterus -bloody nasal discharge and bloody feces -hemoglobinuria relatively uncommon *can't rely on |
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How is Red Water usually diagnosed?
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-usually post mortem (find liver flukes and necrosis of liver)
-history indicates animal is from an endemic region & vaccination is usually inadequate |
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What are 6 post-mortem findings of bacillary hemoglobinuria?
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1) Advanced decomposition
2) Bloody at body orifices 3) Icterus, focal SQ hemorrhages, edema 4) blood tinged fluid in body cavities and pericardium 5) Serosal hemorrhages 6) Characteristic focus of coagulative necrosis in liver |
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What are 4 further diagnostics that can be performed in animals with bacillary hemoglobinuria?
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1) Gram stain impression smears of liver, spleen, blood and abdominal fluid
-large gram + rods -relate to time of death 2) FAB on impression smears of fresh or fixed tissue 3) Toxin testing (usually unnecessary & difficult & expensive) 4) Histopathology: numerous clostridial rods in the hepatic lesion *rarely do further diagnostics |
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What can you do to treat bacillary hemoglobinuria?
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-supportive, transfuse if severe hemolytic anemia
-minimize stress & chances of sudden death *usually don't treat bc die |
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What are 2 ways to prevent bacillary hemoglobinuria?
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1) Burn, bury or remove carcasses
2) Commercial bacterins/ toxoids -monovalent or combination -control for liver flukes -5 to 6 months of protection |
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What animals have the highest prevalence of liver abscesses? Why?
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Cattle: erosion of rumen epithelium from high energy diets inducing lactic acidosis
-so can have 80-90% prevalence in herd if have inappropriate management -usually feedlot animals bc receive high grain diet |
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80-97% of liver abscesses in cattle are caused by what agent?
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F. necrophorum
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How do neonates get liver abscesses?
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Extension of umbilical infection
-umbilical vein gets infected and infection ascends all the way to the liver |
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When do goats most commonly get liver abscesses?
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Usually concurrent disease, especially caseous lymphadenitis
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What agent is most commonly isolated from liver abscesses in goats?
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Cornyebacterium pseudotuberculosis
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When are liver abscesses most commonly identified in cattle?
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At slaughter or necropsy
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What are the clinical signs of liver abscesses in cattle?
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-reduced weight gain and feed efficiency
-weight loss, decreased milk, fever, anorexia *nonspecific signs of infection |
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What are 5 differential diagnoses for liver abscesses in cattle?
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1) Traumatic reticuloperitonitis
2) Parasitism 3) Malnutrition 4) Lymphosarcoma 5) Johne's disease (2-3 years old) |
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What are the 3 clinical signs of horses with liver abscesses?
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1) Weight loss
2) Intermittent colic 3) Intermittent pyrexia |
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What are 2 differential diagnoses for liver abscesses in horses?
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1) Abdominal abscesses
2) Cholelithiasis *rarely see liver abscesses in horses *more signs of intermittent colic |
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What animal most commonly experiences complications due to liver abscesses?
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Cattle
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What are 3 possible complications of liver abscesses?
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1) CVC thrombosis
2) Occasionally compress common bile duct -icterus & photosensitizaton 3) Peritonitis due to abscess rupture |
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What are the clinical signs of an animal that suffered a CVC thrombosis secondary to a liver abscess?
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Shock and sudden death from abscess rupture
-pulmonary thromboembolism w/ epistaxis (from piece breaking off and embolizing) , hemoptysis and anemia |
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**What is a top differential for hemoptysis (coughing up blood) in cattle?
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Liver abscess
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What are 3 components used to diagnose liver abscesses?
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1) Cattle: high risk ration should raise suspicion
-incidence can reach 95% if high grain, limited forage and no adjustment period 2) Lab work 3) Ultrasound useful but restricted by anatomy |
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What are 4 possible abnormal findings on lab work in an animal with a liver abscess?
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1) Neutrophilia or reversed N: L ratio
2) Increased fibrinogen and globulins 3) Anemia from hemoptysis and/ or chronic infection 4) Elevated GGT & AST if active hepatic damage * Liver function tests of limited value, don't run bile acids |
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*Why shouldn't you biopsy a suspected liver abscess?
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Can get peritonitis
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When is the prognosis of cattle with liver abscesses poor? But what can you do to treat liver abscesses in cattle?
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In cattle w overt clinical signs, but fusobacterium is highly susceptible to most antibiotics..
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What is the treatment of liver abscesses in horses?
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Long term antibiotic therapy
-penicillin or ampicillin combined w/ rifampin -metronidazole |
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How can you prevent liver abscess formation?
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Dietary strategies:
-adjust grain over 3-4 weeks -Good fiber source -approved feedlot antibiotics **adjust diets = best |
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What are 4 feedlot approved antibiotics?
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1) bacitracin
2) chlor- or oxy-tetracycline 3) tylosin 4 Virginiamycin **metronidazole is ILLEGAL |
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What are 3 viral hepatic diseases of horses?
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1) Equine herpesvirus 1
2) Equine infectious anemia 3) Equine viral arteritis |
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What does equine herpesvirus 1 do to the liver?
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Hepatocellular necrosis w/ inclusion bodies in aborted or affected foals
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What is a major site of infection of equine infectious anemia?
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Retrovirus that infects Kuppfer cells*
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What are the clinical signs of equine infectious anemia?
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Cyclic fever, anemia, edema, weight loss and icterus from RBC destruction & hepatic necrosis
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How does equine viral arteritis affect the liver?
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Severe infections may cause vascular hepatic damage
*look at clinical case in notes |
