Hepatic disease Flashcards
What can cause acute liver injury/ failure?
Prolonged ischaemia Drugs Toxins Neoplasia Metabolic disorders Infectious disease (e.g. Lepto) Immune-mediated disease
What toxins can cause acute liver injury/ failure?
Aflatoxins Amanita mushrooms Blue-green algae Cycad palms Xylitol
What drugs can cause acute liver injury/ failure?
Phenobarb Paracetemol Oral benzodiazepines (cats) Carprofen Lomustine Mititane Sulphonamides Zonisamide Itra/kenoconzaole Glipizide Methimazole/ carbimazole Rifampicin Tetracycline
Which infections can cause acute liver injury/ failure?
FIP Lepto Infectious Canine Hepatitis Salmonellosis Toxoplasmosis Platynosum fastosum
How can acute liver injury cause hepatic encephalopathy?
Combination of hyperamonaemia, excitatory neurotoxicity, oxidative stress, altered permeability of the blood-brain barrier, inflammation, neurosteroid-induced GABA receptor modulation within the CNS
What can precipitate hepatic encephalopathy?
Hypokalaemia (increases renal tubule ammoniogenesis)
Hyponatraemia (risk factor for cerebral oedema)
Metabolic acidosis (facilitates ammonia diffusion into the CNS)
Can you have normal ammonia levels and hepatic encephalopathy?
Yes
How can you manage seizures caused by hepatic encephalopathy?
Leviteracetam ideally, can also do propofol
There is some evidence that diazepam may play a role in the pathogenesis of HE so avoid if possible
What other treatment should be given for hepatic encephalopathy apart from controlling seizures?
Emergency - warm water cleansing enema (10mL/kg) to reduce the number of ureae-producing bacteria in the colon
Follow with a lactulose retention enema, then oral
Metronidazole (lowered dose of 7.5mg/kg) or ampicillin
Manitol if intracranial pressure is suspected due to cerebral oedema
Avoid excessive protein restriction as this may increase ammonia in the blood due to endogenous protein catabolism (monitor protein levels by measuring albumin). Ideal is a heptaic diet with cottage cheese added
Why/ when give antimicrobial prophylaxis in acute liver injury/ failure?
Secondary infection is a major cause of death
Only give when there is a vasopressor non responsive hypotension, progression or HE, positive culture of infection
Give a broad spec AB
Why give antacids with liver injury/ failure?
High risk of gastro-duodenal ulceration Omeprazole H2 agonist Also sucralfate Evidence that gastric pH is elevated with liver disease, so the effects of an H2 agonist are unclear
Why make vitamin K be low with acute liver injury/ failure? (empiric therapy recommended)
Poor oral intake
intra or extra hepatic cholestasis
AB use may affect the microbiome and reduce vit K2 producing bacteria
What is the prognosis for acute liver injury/ failure?
Low, one study said 14%
Why do animals with liver disease get ascites?
Normally due to portal hypertension
Only sometimes is it hypoalbuminaemia
How do you treat ascites in liver disease?
If low protein - high quality protein, e.g. soya or cottage cheese
Portal hypertension - (tx underlying thing also!) Spironolactone over frusemide, K+ sparing. Can take 2-3 days for effect. Only use frusemide to speed things up.
Do not drain unless it is life threatening (rare)
Why is GI ulceration common with liver disease
Portal hypertension leads to gut wall oedema, leads to ulceration
When should you not use metoclopramide with liver disease
When there is HE
When should maropitant be avoided with liver disease?
Significant liver dysfunction (metabolised by the liver)
What is the antacid of choice for liver disease?
Ranitidine
Which antacid is indicated for paracetemol toxicity?
Cimetidine - involved with P450
What is the antidote for paracetemol toxicity?
N-acetylcysteine - a glutathione precursor.
It binds the toxic metabolite and increases glucoronidaton.
SAM-e also useful to replenish glutathione, which inactivates the toxic metabolite
How do you treat potentiated sulphonamide toxicity?
N-acetylcysteine also useful, treat the signs.
How do you treat phenobarb toxicity?
Some dogs develop hepatocutaneous syndrome on long term therapy
Ideally withdraw and replace with a drug not metabolised by the liver (e.g. KBr)
SAM-e v useful as it is a precursor for antioxidant and detoxifying systems of the liver
What is the typical appearance of hepatocutaneous syndrome on ultrasound
Liver has a swiss cheese appearance
What bacteria are associated with hepatitis?
E.coli Enterococcus Klebsiella Clostridium Faecal Strep Corynebacterium
What should be included in the treatment for suppurative cholangitis?
Manage clinical signs
Antibiotics (penicillins/ cephalosporins/ fluoroquinolones)
Destolit to encourage bile flow
High quality protein diet - normally a critical care diet it best
What causes copper storage disease in bedlington terriers?
Defect in the transport of copper from hepatic lysosomes
How should you treat copper associated hepatitis?
Low copper diet (only prevents further build up)
Anti-oxidants e.g. SAM-e and Vit E
Destolit
Chellation with penicillamine or 2,2,2-tetramine if hepatic copper levels are high or rising
How should you treat chroinc hepatitis?
Palatable high quality protein diet supplemented with zinc, B vitamins, antioxidants. Do not restrict protein unless there are signs of HE
Antibiotics if there is a significant neutrophilic component or ascending infection
Treat ascites as needed
Steroids id there is significant inflammation without fibrosis
Colchicine if there is significant fibrosis
What are the likely US appearances of the following diseases? Hepatitis Nodular hyperplasia Vacuolar hepatopathy Fibrosis Hepatocellular carcinoma Lymphoma Metastasis Necrosis Lipidosis Haemangiosarcoma Steroid hepatopathy Degeneration
Hepatitis - Multifocal, hypoechoic OR Diffuse, heteroechoic
Nodular hyperplasia - Multifocal, hypoechoic
Vacuolar hepatopathy - Diffuse, hyperechoic
Fibrosis - Diffuse, hyperechoic
Hepatocellular carcinoma - Multifocal, heteroechoic
Lymphoma - Multifocal, hypoechoic
Metastasis - Multifocal, hyperechoic
Necrosis - Diffuse, hyperechoic
Lipidosis - Diffuse, hyperechoic
Haemangiosarcoma - Multifocal, heteroechoic
Steroid hepatopathy - Diffuse, hyperechoic
Degeneration - Diffuse, hyperechoic
Outline the use of steroids in liver disease
Used for their immune-modulating/ anti inflammatory or anti fibrotic actions
Very rarely indicated for use in acute liver disease as they are contra-indicated for use when there is portal hypertension
n.b. immune mediated liver disease in dogs has not been convincingly proven yet
When SHOULD steroids be used for liver disease?
There is biopsy evidence of inflammation
There is no fibrosis, or only very mild fibrosis associated with inflammatory infiltrate
Infectious causes have been ruled out as much as possible
When should steroids NOT be used in liver disease?
Known or suspected infectious disease
Advanced, bridging fibrosis or non-inflammatory fibrosis (high risk of serious adverse effects due to the associated portal hypertension)
Ascites - This is normally caused by portal hypertension
Hepatic encephalopathy - steroids lead to protein catabolism and the production of amonia/ other encephalopathic compounds
Acute hepatatis - Animals with acute hepatitis tend to have an infectious or toxic origin and are high risk for ulceration. Only give when there is a specific indication
Why are steroids bad with portal hypertension?
use of steroids precipitates gastrointestinal ulceration
This then precipitates hepatic encephalopathy as a result of bleeding into the intestinal lumen
Steroids also increase water retention
Always avoid dexamethasone as it has high ulcerogenic capacity
What other liver drugs may have anti-inflammatory effects besides steroids?
SAM-e
Destolit
colchicine
Zinv
When are antibiotics used for liver disease?
Tx of HE
When there is infection (bacterial cholangitis is rare)
If there is a suspicion of cholangitis, definitely try to culture as there is a high risk of bacterial resistance in these patients
Outline the use of colchicine
Anti fibrotic
For cases of marked to moderate fibrosis confirmed on biopsy
Monitor animals for bone marrow suppression
Can cause anorexia and d+ than necessitates ceasing of treatment
Unclear how effective it is in dogs - good in people
Would require repeat biopsy to assess response
alkaloid that binds tubulin and has the potential to reverse fibrosis
When is metronidazole useful
Very effective agains anaerobes
Often used in combination with ampicillin/ amox
Reduce the dose to 7.5mg/kg as it is metabolised by the liver
Also for HE
When are fluoroquinolones useful?
For bacterial cholangitis or when gram negatives are suspected
Poor agains anaerobes or strep
Good penetration in liver and bile
Do not use in growing dogs
Never use enrofloxacin in cats due to retinal damage
Which antibiotics that rely on hepatic clearance or are hepatotoxic should be avoided?
Tetracyclines
Sulphonamides
Chloramphenicol
Erythromycin
What antioxidants are there?
Vitamin E Silymarin SAM-e Zinc Logical to use but no clear evidence that they improve the quality of life of the animal/ survival
Outline the use of SAM-e
Increases hepatic and RBC glutathione levels
Especially good for toxic hepatopathies (e.g. phenobarb), may also be good for steroid hepatopathis
Indicated for all types of liver disease, esp also for biliary stasis
Outline the use of vitamin E
Effective anti-oxidant
Use in cases of copper storage disease as levels of vitamin E are reduced in hepatocytes
What is Ursodeoxycholic acid?
Bile acid modifyer
Hydrophilic bile acid that displaces toxic hydrophobic bile acids and stimulates bile flow (ie, it is a choleretic).
This reduces cell damage and oxidative stress resulting from the retention of bile acids in the liver
Also an immune-modulator
Also shows antioxidant activity with a synergistic action with SAM-e and vitamin E
Indicated in all forms of liver disease, although contra-indicated in complete bile duct obstruction
What copper chelators are there (for copper storage disease)
Penicillamine is the most commonly used, however can take weeks to months for an effect
Zinc can be used as a prophylactic
Also 2,2,2-tetramine tetrahydrochloride (2,2,2-T) - not available in the UK
All have side effects, use with caution
Outline palatability/ times requirements for feeding a liver patient
Feed a palatable diet little and often (four to six times a day) as many animals with liver disease may be
anorexic.
Feeding little and often minimises hepatic work and signs of encephalopathy
Outline the protein requirements for a liver patient
Most dogs with liver disease have increased protein requirements.
Highly digestible, high-quality protein should be fed in normal amounts
Consider supplementation with cottage
cheese, chicken or soya when using a commercial
reduced-protein hepatic diet.
White fish should be avoided as it is high in purines. Protein should only be restricted when there is HE Serum albumin concentrations should be monitored to allow adjustment of dietary protein levels
Outline the carb requirements of a liver diet
Dogs with liver disease have impaired carbohydrate metabolism.
Highly digestible complex carbohydrates
should be fed (eg, rice, potato or pasta)
Outline the fat requirements of a hepatic patient
Normal levels unless steatorrhoea develops
Outline the fibre requirements of a hepatic patient
Fermentable fibre is helpful in animals with hepatic encephalopathy as it acidifies the colon and so
traps ammonia.
It also increases nitrogen incorporation into bacteria and reduces bacterial ammonia production.
Non-fermentable fibre helpful in preventing constipation, a predisposing factor for
hepatic encephalopathy.
Lactulose is a synthetic disaccharide that acts as a soluble fibre
Outline the feeding of zinc and copper in a hepatic patient
Zinc deficiency is common in humans with chronic liver disease, thought to occur in dogs.
Zinc supplementation reduces encephalopathy and reduces copper absorption from the gut and copper
availability in the liver. It may also have anti-inflammatory, antifibrotic and antioxidant effects
Increased concentrations of copper can be seen in some liver diseases, intake should be
restricted. This includes not feeding water from copper pipes in soft water areas
Outline fat soluble vitamin supplementation for liver patients
DAKE
Vitamin E is an antioxidant and can be supplemented in cases of liver disease
Vitamin K supplementation may occasionally be necessary if clotting times are prolonged, especially preceding a biopsy. Should be given by the parenteral route .
Vitamins A and D should not be supplemented. Vitamin A can cause hepatic damage and vitamin D supplementation can cause calcification in tissues
Outline water soluble vitamin supplementation in heptatic patients
Vitamin B should be supplemented as there can be increased loss due to polydipsia/polyuria. It is recommended that dogs with liver disease receive a double dose of B vitamins.
Vitamin C should not be supplemented as ascorbate can increase the tissue damage associated with metals in cases of liver disease
What is cholestasis?
Clinical syndrome of impaired bile flow. Not a disease itself
2 types - intra and extrahepatic
Intra - at the level of the hepatocytes/ bili canaliculi/ bile ductuli
Extra - obstruction of the CBD
What can cause EHBDO?
Cholangitis Cholecystitis Impaired contractility of the gall bladder Pancreatitis Biliary neoplasia GI disease Biliary mucocoeles
What are the clinical signs of EHBDO?
Non specific Abdominal pain Vomiting Dehydration Nausea Anorexia Weight loss Lethargy possible pyrexia D+ Icterus D+
How can you dx EHBDO?
US - if intrahepatic bile ducts in cats are seen, they are dilated
If the CBD is >5mm, very likely there is an EHBDO
Can’t use gall bladder size as this varies a lot
Bloods - High ALP, bilirubin, bile acids
How do you Tx EHBDO?
Depends on the cause
If doing biopsies of the abdominal organs, when should liver biopsies be taken?
Early, hepatocellular damage resultsfrom prolonged GA/ handling of the intestines
What is the most likely route of diagnosis for neutrophilic cholangitis?
Bile evaluation (can be from cholecystocentesis with a 22g needle under ultrasound guidance
Often cannot see anything abnormal with the GB on US
Bloods can be noral of have high liver enzymes
Compare ALT and ALKP measurements in the dog and cat
Much more sensitive in the dog - many cats will not get increases in liver enzymes with hepatic disease
More specific in the cat
In cats the most sensitive liver enzyme is GGT, often not on a routine profile
ALT and ALKP half lives in cat = 6 hours, in dog is 52/ 70
When are Bile Acids raised?
If marked - vascular abnormality/ liver failure
If mild, less specific, can be primary or secondary disease, eg. cushings
What do target signs in the liver on US suggest?
Mets
How should the spleen look compared to the liver on US?
Spleen should be hyperechoic
How would hepatic lipidosis look on us (only one that is easy-ish to diagnose if rest of the clinical picture fits)
Hyperechoic, rounded edges
What does a honeycomb spleen suggest?
Lymphoma
What would suggest GB wall disease on US
> 1mm thickness in cats,
>2-3mm in dogs
Is US good to assess bile ducts?
Good for large bile ducts, not for small?
How significant is sludge in the gall bladder?
Cats - suggests an issue
NAD in dogs
What diseases may be diagnosable on FNA of the liver?
Lymphoma/ other round cell disease
Vacuolar hepatopathy
What can cause reactive liver disease?
Cushings GI disease CHF anaemia Hypoxia sepsis Diabetes Pancreatitis
What is chronic hepatitis?
Sterile inflammatory disorder with no discernible cause
More common in springer spaniels/ labs
What is seen on histo with chronic hepatitis?
No infectious agents/ massive copper accumulation/drugs etc
Hepatocellular necrosis and apoptosis
Variable mononuclear or mixed inflammatory infiltrates
Regeneration and fibrosis
What is seen on US with chronic hepatitis?
Often nothing
Therefore samples need to be taken!
How do you treat chronic hepatitis?
Not good evidence for the use of 1mg/kg SID pred, but recommended by WSAVA. Taper dose. Unclear which action of the steroids may be helping
Can also include cyclosporin/ azathioprine/ mycophenalate (best evidence for ciclosporine)
Destolit should be useful
Less evidence for anti-oxidants as there shouldn’t be oxidative damage
Which sex is more common to get immune mediated diseases in?
Female
What are the negative prognostic indicators for chronic hepatitis?
Coagulopathies Ascites Anorexia High Tbili Cirrhosis
How can you assess response to treatment with chronic hepatitis?
Clinical improvement
Improvement in bloods (although remember now on preds so may not go back 100%
Can do repeat biopsy
What happens in HE?
Ammonia levels can be normal so that is not the only cause - must be multiple pathways
Acute liver failure or shunts
Manganese involved
Oedema leads to astrocyte swelling - neurotransmitter dysregulation
What can trigger HE?
dehydration high protein (meal or GI bleeding) Azotaemia Low K or Na Alkalosis Dietary indiscretion
How low does alb need to be to cause ascites
Approx 18
What is silymarin (milk thistle)?
antioxidaNT
Poor bioavailability (meant to be best in denamarin)
Decreases oxidative damage and therefore fibrosis
Increases glutathione levels
Outline ALT
In high concentrations in the cytoplasm and mitochondraa of hepatocytes
Marker of hepatocellular injury - (can be reversible injury)
Also in muscle - correspond with CK if concerned re muscle
Levels increase within 12 hours of injury and peak 24-48 hours after
What hepatic causes of rises of ALT/ AST are there?
Drug-induced liver injury
Hepatic lipidosis (cats)
Infectious: for example, ascending enteric bacterial infection, feline infectious peritonitis,
schistosomiasis, leptospirosis
Inflammatory: copper-associated chronic hepatitis, idiopathic chronic hepatitis, cholangitis,
gall bladder mucocele
Lysosomal storage disease
Neoplasia (primary or metastatic)
Nodular hyperplasia
Portosystemic shunt (congenital or acquired)
Toxin ingestion: for example, aflatoxin, amanita mushroom, blue-green algae, copper,
herbicides, insecticides, iron, sago palm, zinc, xylitol
Trauma
Vacuolar hepatopathy (idiopathic)
Outline AST
Marker of hepatocellular damage
Less specific for the liver cf ALT
Also in the brain, kidney, RBCs, skeletal muscle, cardiac tissue
half life of 12 hours in dogs and 1.5 hours in cats
What are possible secondary causes of high ALT/ AST?
Diabetes mellitus Enteritis Hemolysis (AST) Hyperthyroidism (cats) Hypoxia: cardiac disease, hepatic thrombosis, anemia Hypothyroidism (dogs) Myopathy (more likely AST) Pancreatitis/pancreatic neoplasia Peritonitis Septicemia Vacuolar hepatopathy (secondary to exogenous/endogenous glucocorticoids)
Outline ALP
Associated with the cell membrane in multiple tissues including hepatocytes
Isoenzymes in bone, placenta, intestines, kidney, only steroid, bone and liver important in dog, only bone and liver in cat
Half life in dogs = 70 hours, 6 hours in the cat
Often related to cholestatic disorders
Increase in ALP is often delayed compared with ALT/AST
What can cause HEPATIC increases in ALP?
Biliary tract disease Biliary neoplasia Cholelithiasis Cholecystitis Gall bladder mucocele Hepatic parenchymal disease Cholangitis Chronic hepatitis (idiopathic and copper associated) Hepatic lipidosis (cats) Hepatic neoplasia: primary or metastatic Nodular hyperplasia Toxin ingestion: for example, aflatoxin, amanita mushroom, blue-green algae, copper, herbicides, insecticides, iron, sago palm, zinc, xylitol Vacuolar hepatopathy (idiopathic)
What non-hepatic things can cause increases in ALatic
Bone neoplasia/osteolytic disease Chronic passive congestion Diabetes mellitus Exogenous/endogenous glucocorticoids (glucocorticoid-induced isoenzyme in dogs, also cause vacuolar hepatopathy) Growing animal Hyperthyroidism (cats) Hypothyroidism (dogs) Pancreatitis/pancreatic neoplasia Septicemia
Outline GGT
Cholestasis/ biliary hyperplasia
Possibly more sensitive than ALP in cats (except in hepatic lipidosis where ALP is high and GGT is not
GGT in dogs is more specific but less sensitive
Half life of 70 hours in the dog
Outline bilirubin
Mostly generated from the removal of senescent RBCs
Prehepatic, hepatic or post hepatic
Hepatic is caused by decrease in hepatocyte function and intrahepatic cholestasis - but has to be significant disease before levels rise so is not sensitive
Post hepatic = EHBDO (mucocoeles, pancreatitis, neoplasia, bacterial cholecystitis, cholelithiasis, Traumatic rupture of bile duct or gallbladder)
How is ammonia produced?
In the intestines via catabolism of glutamine by enterocytes and bacterial deamination of dietary protein and GI haemorrhage
Outline measurement/ meaning of ammonia levels
> 70% function needs to be gone before it goes up
Not influenced by cholestasis or hepatic disorders that do not alter the portosystemic circulation or significantly reduce hepatic functional mass
Sensitivity for diagnosing shunts - 81-100%
Can also be caused by enzyme deficiencies (genetic or acquired secondary to b12 or arginine deficiency)
Has to be analysed within 30 minutes
May see ammonium biurate crystals on sediment
What are the common pre hepatic causes of high bilirubin?
(Haemolysis) Hemoparasites Heinz-body hemolytic anemia Hypophosphatemia-induced hemolytic anemia Immune-mediated hemolytic anemia Neonatal isoerythrolysis Transfusion reaction Zinc toxicity
What are the common hepatic causes of high bilirubin?
Dogs
Acute liver injury: drug-induced liver injury, hepatotoxins
Chronic hepatitis (idiopathic and copper associated)
Hepatic necrosis
Infectious disease: for example, leptospirosis, hepatozoonosis
Round cell neoplasia
Septicemia
Cats:
Cholangitis
Hepatic lipidosis
Infectious disease: for example, feline infectious peritonitis, toxoplasmosis, cytauxzoonosis
Round cell neoplasia
Sepsis
What is the role of bile acids?
Enhance solubilisation of lipids in the intestine
facilitate digestion and absorpion of fats and lipid soluble vitamins
When are BA test results unreliable?
If have ileal disease or cholecystectomy
What do raised BA results mean?
Hepatic dysfunction, shunt, or cholestasis - therefore if there are other measures of cholestasis (e.g. high bilirubin) then there is no point in testing
What can cause low cholesterol?
Severe hepatic insufficiency Malabsorption/ maldigestion Decreased dietary intake addisons Protein losing enteropathy/ nephropathy
What are the most common causes of low albumin?
fully made in the liver
PLE/ PLN
Severe liver insufficiency
Severe exudative skin disease
Why are there coagulopathies with liver disease?
Production of vitamin K
Site of activation for vitamin K dependent clotting factors (II, VII, IX, X, protein C)
Cholestasis may lead to vitamin K malabsorption
Makes fibrinogen
What haematology changes may be seen with liver disease?
acanthocytes
echinocytes
target cells
stomatocytes
Shistocytes if there are microangiopathic chanes due to DIC or hepatic neoplasia
May see a thrombocytopaenia due to decreased production of thrombopoietin
How important is hyperbilirubinaemia on a dipstick?
Cat - always important
Can be 2+ normal in male dogs
What may measurement of Protein C be useful for?
Higher activity of protein C suggest microvascular dysplasia over a shunt
When may you see a hypochromic microcytic anaemia?
PSS
Iron deficiency
Is GI h+ more common in intra or extra hepatic shunts?
Intra
Is ascites often seen in PSSs?
No - in congenital PSS, there is portal hyPOtension
How does lactulose work?
Accidifies the intestine (ammonium is hard to diffuse)
Increases gut transit time
Provides a non-protein substrate for GI bacteria
How much of oncotic pressure is controlled by albumin?
80%
How common is high bilirubin PSS?
Rare in congenital, more common in acquired
What bleeding disorders can occur with liver disease and why?
Liver makes inhibitor proteins to prevent excess h+
Also makes clotting proteins
Can get thrombosis or h+
Sponatnous h+ rare but lab abnormalities are common
What is the best blood product for clotting problems?
FFP
Stored whole blood is low in factors V and VIII
What are the differentials for hepatomegaly?
Engorgement - rCHF/ pericardial effusion/ vascular or lymphatic engorgement
Increased hepatocyte size - vacualor hepatopathy, e.g. cushings
Infiltrate - inflammatory or neoplastic
Outline how useful FNAs are
FNAs and biopsies have variable agreement
Vacuolar hepatopathy easiest to dx but also most common false dx
Can’ assess architecture/ fibrosis
Outline hepatic lymphoma
Rare, normally T cell
MST 63d
High bili and low alb poor prognosis
Lots of chemo drugs are metabolised by the liver
What type of bacteria are isolated in cholangitis
Mostly aerobic, enteric
When can you clincally see jaundice?
> 30
Outline the movement of bilirubin
Produced by macrophages breaking down RBC
Made into conjugated form in the liver
Broken down the urobilinogen in the intestines by bacteria
Further along made into stercobilin (in f+) and urobilin which small amount is renally excreted, most recycled through portal system
What type of bilirubin is present in pre-hepatic disease
Starts off as unconjugated, then there is a mix with conjugated
What are the ddx for prehepatic jaundice?
IMHA
infectious (erlichia, babesia, FIA)
Toxins - paracetemol, onion, Pb, Cu, methylene blue
Propylene glycol
Neoplasia - haemangiosarcoma
DIC
Breed specific enzyme deficiencies - phosphofructokinase in springers, pyruvate kinase in beagles, basenjis, abyssinians and somali cats
Outline how PCV can help indicate something may be pre hepatic
Need to see a 10% drop in PC to get icterus
Normally PCV in <20% if prehepatic (could still be others though)
How may liver enzymes change in cirrhosis?
Small elevations may be important
How do you analyse enzyme changes with phenobarb
Induces liver enzyme synthesis
Up to 5x is normal
Shouldn’t see changes to BA or liver function tests if not causing damage
What can cause changes in folate measurements?
High - supplement, SIBO, EPI, artefact with haemolysis
Low - Dietary deficiency, proximal SI dz
What can cause changes in B12 measurements?
High - supplement
Low - dietary deficiency, SIBO, EPI, distal SI disease
