1. Effusion
1.1. Increased fluid in abdominal/thoracic cavity - not a disease in itself
1.1.1. Analysis - different fluid types - diagnostics, specific aetiologies
1.1.1.1. Collect in EDTA - counts (no clotting), cytology and protein
1.1.1.2. Collect in serum (plain) tube - biochemical tests or culture - not gel tubes
1.1.1.3. Total Nucleated Cell Count (TNCC)
1.1.1.3.1. TNCC and total protein: classification
1.1.1.4. Cell identification and morphology
1.1.1.5. Enzymes (amylase, lipase) Urea, Creatinine Cholesterol, Triglycerides
1.1.1.6. Normal: low volume, clear, straw colour, total protein 25-30 g/L, Nucleated cell count <3 x 10e9/L, Mesothelial cells/macrophages, few cells on cytology
1.1.1.6.1. Regulation: hydrostatic pressure, colloid osmotic pressure (albumin), permeability of capillary wall, lymphatic drainage
1.1.1.6.2. Modified Transudate/Exudate
1.1.1.6.3. Equine peritoneal fluid
2. Lab Diagnostics
2.1. Liver Disease
2.1.1. Enzymes - indicating hepatocellular damage Not specific enough to determine underlying cause - need FNA or biopsy
2.1.1.1. Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Sorbitol dehydrogenase (SDH) Glutamate dehydrogenase (GLDH)
2.1.1.1.1. leaked from hepatocytes, indicate damage/necrosis of these cells
2.1.1.1.2. Dogs and Cats - ALT Increaes within 12 hours of injury, peaks at 1-2 days, decrease over 2-3 weeks Can be derived from muscle (like AST)
2.1.1.1.3. Large animals - SDH or GLDH - more liver specific in LA vs ALT - rare in SA
2.1.1.2. Cholestasis, obstruction to bile flow Regurge of biliary substances into blood Alkaline phophatase (ALP) Gammaglutamyltransferase (GGT)
2.1.1.2.1. ALP - from bile duct epithelium Also in bone, so in young growing animal May be induced by steroids in dogs Change in cats is significant!
2.1.1.2.2. GGT - from bile duct epithalium More sensitive to cholestasis in LA In colostrum, so in nursing animals Also found in renal tubular cells, may be found in urine (not blood) with renal tubular damage
2.1.2. Hepatic function measures
2.1.2.1. Bilirubin
2.1.2.1.1. From spleen to liver - conjugation - bile - gut, urobilinogen- renal excretion
2.1.2.2. Ammonia and urea
2.1.2.2.1. Products from protein metabolism Ammonia derived from gut, travel to liver via portal system - converted into urea
2.1.2.3. Glucose
2.1.2.3.1. Production of glucose in liver Not that sensitive - decreases in end-stage liver disease, but hypoglycaemia could also mean neoplasia and bacterial sepsis Seen in stress and diabetes mellitus
2.1.2.4. Cholesterol
2.1.2.4.1. Post prandial - increases Also inc. with endocrine disorders (DMell, hyperadrenocorticism) Varies inversely with T4 (inc. with hypothyroidism, dec. with hyper)
2.1.2.5. Bile acids
2.1.2.5.1. Emulsifies fat, recycled as energetically expensive to build, excreted into bile duct, reabsorbed via enterohepatic circulation - little acids found normally from normal circulation
2.1.3. CBC - Acanthocytosis (altered RBC, lipid metabolism defect, haemangiosarcoma) Anaemia (hepatitis, functional mass, inflammatory) Codocytosis (functional mass, altered erythrocyte membrane) Microcytosis (functional mass, portosystemic shunt, transferirin production and delivery of iron to RBC precursors)
2.1.4. UA - ammonia biurate crystals, bilirubinuria, hyposthenuria/isosthenuria, urate crystalluria
2.1.5. Coagulation assay - PTT/PT (vitamin-K absorption via gut and coagulation/production of other clotting factors built in liver Faecal - steatorrhoea - defective lipid digestion as bile acids not delivered to GI Transudate - Na and H2O retention, portal hypertension, lymph drainage
3. Hepatic and Pancreatic pathology
3.1. Intoxication
3.1.1. Acute = haemorrhage, dec. synthesis of clotting factors and increased consumption by damaged liver
3.1.2. Chronic = regeneration and repair - fibrosis, biliary hyperplasia Toxins (ragwort, copper), or drugs
3.2. Circulatory
3.2.1. Centrilobular necrosis
3.2.1.1. Ischaemia, metabolic/toxic damage
3.2.1.1.1. Zonal = ischaemia
3.2.1.1.2. Random = Viral, bacterial, itis
3.2.1.1.3. Focally extensive = bacterial
3.2.1.1.4. Massive = toxicity, injury
3.2.2. Passive venous congestion
3.2.2.1. Circulatory Disorder RSHF (acute/chronic)
3.2.2.1.1. Enlarged, rounded edges = nutmeg liver (lobular)
3.2.2.1.2. Microscopically: venules, sinusoids congested, centrilobular hepatic atropy, periportal fatty change (pale red)
3.3. Degenerative
3.3.1. Vacuolar hepatopathies
3.3.1.1. Swelling, vacuolation of hepatocytes Hydropic, lipidosis, glycogenosis Zonal or diffuse
3.3.1.1.1. Hydropic = common, non-specific, reversible Hypoxia, mild toxicity, metabolic stress
3.3.1.1.2. Glycogenosis = HAC, steroids
3.3.2. Lipidosis (fatty liver)
3.3.2.1. Obesity Starvation Energy demand inc. e.g. pregnancy Diseases: diabetes mellitus, ketosis, preg. toxaemia
3.3.2.1.1. Dec. FA complexing, decreased low density lipoproteins
3.3.3. Amyloidosis
3.3.3.1. Primary, secondary, endocrinopathy Enlarged, friable liver
3.3.3.1.1. Stains green birefringance with congo red
3.3.4. Fibrosis
3.3.4.1. Inflammatory, scarring following necrosis, Cirrhosis (Degen. and regen.) - end stage liver
3.4. Congenital/Developmental Disorders
3.4.1. Portosystemic shunt
3.4.1.1. Portal blood bypasses liver - atrophic Congenital, or acquired (secondary to fibrosis, or thin wall shunts)
3.4.2. Developmental pancreatic hypoplasia
3.4.2.1. GSD, calves
3.4.2.2. Steatorrhoea, diarrhoea (fatty faeces) Loss of condition despite polyphagic and pot bellied Distended intestines - fatty ingesta Lack of abdominal fat
3.5. Parasites
3.5.1. Usually incidental (except liver fluke) Ascaris suum - large roundworm - milk spots in liver due to migration Strongyle migration in horses Fibrous tags on liver surface and diaphragm
3.6. Hyperplastic disease
3.6.1. Nodular hyperplasia (older dogs)
3.6.1.1. Portal areas still visible
3.6.1.2. Compression of adjacent tissue
3.6.2. Larger cells - contain more glycogen?
3.6.3. Pancreatic hyperplasia
3.6.3.1. Nodular hyperplasia common - clinically insignificant
3.7. Inflammation
3.7.1. Hepatitis often infectious (parenchyma inflammation)
3.7.2. Cholangitis - bile ducts
3.7.2.1. Infection (e.g. Salmonellosis)
3.7.2.2. Immune mediated e.g. cats
3.7.3. Cholangohepatitis
3.7.4. Acute
3.7.4.1. Necrosis then inflammation, then regeneration, repair, fibrosis, scarring, encapsulation (abscessation) - persistence by granulomatous disesae
3.7.4.1.1. Dogs + cats: Leptospira (not common, vaccination) Adenovirus (CAV-1) - vaccinated Bacterial endotoxaemia/septicaemia Liver fluke (acute/chronic damage, neoplasia risk) Toxic/trug induced Neoplasia (diffuse infiltrate, lymphoma) Genetic - acute necrosis with Cu storage disease
3.7.4.1.2. Cats: Inflammatory (cholangitis, may include gut, pancreas - bacterial susceptibility) Neoplastic Lipidosis (obese) Infectious - Bact, toxoplasmosis, FIP (coronavirus) Toxic/drug
3.7.5. Viral
3.7.5.1. Young, unvaccinated animals
3.7.5.1.1. Adenovirus - Canine infectious hepatitis
3.7.5.1.2. Herpes virus - EHV-1, infectious bovine rhinotracheitis, feline viral rhinotracheitis, Aujeszkey's disease Feline infectious peritonitis (FIP) - mutated coronavirus
3.7.5.1.3. Infectious canine hepatitis
3.7.6. Bacterial - direct, haematogenous, abscessation
3.7.6.1. Fusobacterium necrophorum - umbilical (calves), rumenitis (abscesses from necrosis)
3.7.6.1.1. Focally extensive necrosis, abscessation, anaerobic
3.7.6.2. Clostridium novyi type B - Black's Disease Sheep - liver fluke precipitates, subcut. venous congestion, oedema - anaerobic conditions
3.7.6.2.1. Fibrinous peritoneal, pericardial. thoracic fluid
3.7.6.2.2. Pale foci necrosis, surroudned by haemorrhage (cytology)
3.7.6.3. Bacillary haemaglobinuria - Clostridium haemolyticum - Cattle, sheep, similar pathogenesis to novyi
3.7.6.3.1. Anaemia, jaundice, haemoglobinuria, focal extensive hepatic necrosis, Hb staining of kidneys
3.7.6.4. Clostridium pilforme - Tyzzer's Disease - Rodents, young foals, immunosuppressed cats/dogs
3.7.6.4.1. Wheat sheaf colonies, intestinal lesions
3.7.6.5. Salmonellosis
3.7.6.5.1. Fever, dehydration, diarrhoea, haemorrihagic ileitis, pin-point necrosis, parathyroid nodules
3.7.7. Acute pancreatitis
3.7.7.1. Release TNF lipase and amylase - fat necrosis, chalk-like, saponification, reddening
3.7.8. Chronic pancreatitiis
3.7.8.1. Bouts of acute - replace and fibrosis Exocrine panc. insufficiency - steatorrhoea and loss of condition
3.7.8.1.1. May be subclinical in cats and horses
3.8. Gall bladder and extrahepatic bile duct
3.8.1. Inflammation (Cholecystitis)
3.8.1.1. Salmonellosis , infectious canine hepatitis
3.8.1.2. Hyperplasia of mucosa as reaction
3.8.2. Choleliths - incidental
3.8.3. Rupture = bile peritonitis
3.9. Neoplasm
3.9.1. Primary
3.9.1.1. Hepatocytes
3.9.1.1.1. Hepatoma, hepatocellular carcinoma
3.9.1.1.2. Biliary epithelium
3.9.2. Metastatic
3.9.2.1. Haemangiosarcoma (large breeds
3.9.2.2. Common metastatic site
3.9.3. Pancreatic neoplasia
3.9.3.1. Adenoma (rare) Carcinoma (cats and dogs)
3.9.3.1.1. Highly invasive, metastatic to liver, peritoneum, lymph nodes, spleen, adrenals
3.10. Chronic hepatopathies
3.10.1. Inflammatory (idiopathic, acute progression, Eos and granulomatous, hepatitis - Doberman) Cirrhosis - reduced tissue function Neoplastic (primary/secondary) Drug induced (glucocorticoid) Developmental/congenital (shunt, hypoplasia, Cu storage disease)