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Liver, Response to injury, PANCREASE, presence of inflammatory cells…

- - - - lobular necrosis
        
        least common
    - - active in detoxification
      - lowest oxygen
      - prone to toxic + hypoxic injury
      - lobular necrosis
        
        hypoxia, toxicity, acute heart
        failure, viruses, slow (agonal) death
    - - prone to direct toxic injury
      - Lobular necrosis
        
        uncommon, direct acting toxins
    - - Paracentral
        
        coagulative necrosis due to infarction
  - - - ammonia toxicity
        
        damage BBB
        
        death due to cerebral edema
      - Variable neurologic signs
        ▪ Ruminants: blindness, dullness
        ▪ Horses: mania
        ▪ Dogs and cats: subtle
    - - impaired bile secretion/flow
        
        Hepatocellular
        
        Obstructive
    - - yellow pigmentation of tissues due to excess plasma bile pigments
        
        prehepatic (ex. hemolysis), hepatic (altered function), orposthepatic (ex. obstruction)
      - Blockage of the main bile duct leads to jaundice
    - - primary
        
        unchanged native compounds that were ingested
      - Hepatogenous
        
        cholestasis in herbivores eating green forages
  - - - Aberrant connection between the portal vein and vena cava
        (portocaval) or azygous vein (portoazygous)
      - always a single vessel
    - - portal hypoplasia beyond the shunt
      - Small dogs, cats
    - - Persistent patent ductus venosus
      - Large dogs
  - - - anything that causes
        portal hypertension
      - Multiple, small, tortuous, thin-walled vessels
  - - - Adenoma
        
        single, spherical, well demarcated, and
        not clinically significant
      - carcinoma
        
        Poorly demarcated, May be single, nodular, or diffuse, Commonly invade veins
    - - Pale, often umbilicated, almost always multiple or diffuse
      - Very invasive, commonly metastasize to lymph nodes and lungs
      - cause carcinomatosis in cats
    - - arise in liver or be metastatic
- - - - look at ketones; AST + ALP good for cats; GLDH in horses, cattle, llamas
  - - - GGT
        
        Cholestasis
        • Most GGT is from biliary tree
        • More specific for cholestasis than ALP, esp. LA and cats
        • (i.e., fewer things cause it to increase, it’s not present in bone, etc.)
        • Takes longer to increase than ALP
        • Steroid induction happens in dogs – mild
        
        DDX for INC
        
        Post colostrum
        • Puppies, lambs, calves
        Foals mild increases – not colostral origin
        Acute hepatic injury:
        • Membrane fragment release
        • Dogs with adverse reaction to anticonvulsant medication
        • May see prior to increases in ALT
        • Horse & cow with pyrrolizidine alkaloid toxicity
      - ALP
        
        choleostasis, dramatic inc in dogs, less in cats; LA not as reliable
        
        Endogenous / exogenous corticosteroids induction in dogs Anticonvulsant therapy (e.g., phenobarbital) & phenylbutazone
        Hepatic lipidosis / hyperthyroidism in cats
        • ALP is not liver-specific:
        • Present in: liver, bone, intestine, kidney, placenta, WBCs
        
        bone alp
        
        • Young animals (growing) 2-3x adult value (higher in foals)
        • Adult animals – 2-4x increase with:
        Neoplasia involving bone
        Osteomyelitis
        Hyperparathyroidsm
        Hyperthyroidism, etc
        
        DDX for inc
        
        Dogs – drug induction:
        • Corticosteroids – exogenous / endogenous
        • 7 d exposure for ALP to increase from corticosteroids
        • Oral, parenteral, topical, otic, ophthalmic
        • Hyperadrenocorticism
        • ± increased ALT
        • Corticosteroid ALP (cALP), GGT may also increase
        • Anticonvulsants / NSAIDs
        • Phenobarbital, phenytoin, primidone
        • Phenylbutazone
        • GGT not increased
        
        Cats with ↑ ALP but normal bilirubin
        • ALP and/or ALT – hyperthyroidism
        • 90% of cats with hyperthyroidism will have an increase
        in one or the other of ALP or ALT
        Liver Exocrine Pancreas Beeler-Marfisi - VETM*4490 32
        Feldman & Nelson, 3 rd Ed.
        • ALP and AST – hepatic lipidosis
        
        bone lysis
  - - - GLDH
        
        reliable in horses, bovine and birds
        
        specific and sensitive for hepatocellular injury
      - AST
        
        not liver specific parallels ALT; if dmg stops dec over 2-3 weeks
        
        reliable in cat, dog, horse, bovine
      - ALT
        
        inc 12h after injury, reliable in cats and dogs
        
        investigate if
        
        cats with lymphoplasmacytic hepatitis
        
        chronic hepatitis in middle age dogs
        
        young dog with PSS or poor oral health
- - - - Cholestasis in horses: horse off feed for 12 hours; inc bilirubin = inc ubili
- - - - serum bile acids
        
        made from cholesterol, stored in gall bladder; aid in absorption of fat and fat soluble vitamins
        
        Enterohepatic recirculation-> very efficiently cleared from portal circulation, secreted into biliary system
        
        measure when
        
        liver enzymes increased but bilirubin normal
        
        Don’t do if icteric – increased in any animal with cholestasis
        
        monitor liver function in cases of known hepatic disease
        
        intrepretation in cats and dogs
        
        normal<15
        
        liver dz >25
        
        equivocal 15-25
        
        interpretation in horses, ruminants, llama
        
        horses marked inc in SBA 40-100; a lot of variation in cows
        
        Hepatic necrosis, hepatic lipidosis, neoplasia, cirrhosis
        
        best test for detection of
        hepatobiliary Dz in cattle
        
        increases when
        
        deviation of portal circulation (PSS, Cirrhosis)
        
        dec in hepatocyte uptake (diffuse hepatocellular dz)
        
        dec bile excretion with subsequent regurg into blood (hepatic/post hepatic cholestais)
- - - - Fusobacterium necrophorum
      - Multifocal dry areas of coagulative necrosis surrounded by hemorrhage
    - - systemic disease with acute jaundice, cholestasis, renal failure
    - - common in feedlot cattle
    - - Clostridium novyi type B
      - Congested SQ vessels; Abdominal fluid clots on exposure to air; Yellow-white liver necrosis with red rim
  - - - milder than fasciola
    - - fatal anemia, black dz.
      - Adults live in bile ducts, causing
        dilation and fibrosis
  - - - Sudden death with no signs or anorexia
      - reportable dz
  - - - mix of inflammation, apoptosis/necrosis, regeneration
    - - chronic necroinflammatory disease lasting > 6 months
      - copper accumulation in dogs
        
        COMMD1 mutation in Bedlington terrier: impaired copper excretion
    - - neutrophilic
        
        part of triaditis and bile obstruction
      - lymphocytic
        
        slowly progressive
    - - form in gallbladder, mix of cholesterol, bile pigment, salts
      - severe irritation (bile peritonitis)
- - - - Lytic
        
        disintegrating cells, later stages
      - coagulative
        
        intact cells, common in acute toxicity
- - - - hepatic encephalopathy, ascites, icterus, photosensitization, coagulopathy, hepatocutaneous syndrome
- - - - hepatotoxicity in young pigs if accidentally overdosed
    - - sheep are very sensitive to copper toxicity
    - - Microcystin-LR toxin disrupts the cytoskeleton and causes necrosis
    - - cats - acetominophen
    - - Dose-related, predictable, reproducible
    - - Less dose-related, unpredictable
- - - - Associated with high fat, low protein diets
      - terriers!!!!
      - peripancreatic adipose saponification
        (yellow flecks) accompanied by swelling and edema,
        hemorrhages in and around the pancreas, fibrin
  - - - Very common, grey-white and
        firm, usually incidental
  - - - Rare, usually incidental, unlikely
        to progress to carcinoma
        Look more like normal
        parenchyma than nodular
        hyperplasia
    - - Rare in all species, female > male
        May be scirrhous, often contain
        necrosis
        Poor prognosis