Dogs and Cats 18 Flashcards
What are some causes of liver biochem changes but aren’t primary liver disease
1) Hyperthyroidism
○ 80% affected cats have increase enzymes (esp ALT)
2) Hyperadrenocorticism
○ Glycogen deposition -> vacuolar hepatopathy
○ Reversible, mild changes in BAS, INCREASE in ALP
3) Diabetes mellitus
○ Lipid deposition
4) Right-sided CHF
○ Diffuse hepatomegaly
5) Cholestasis of sepsis
○ Increase in bilirubin/ALP (functional ileus of bile duct) but ALT etc OK
○ Reactive to an issue elsewhere in the body
6) Acute pancreatitis
7) IBD
○ 25% dogs/cats with IBD have increase liver enzymes
Haematology and diagnostic imaging results that suggest liver disease
- Haematology
○ Anaemia (rules out pre-hepatic)
○ Thrombocytopaenia
○ Eosinophilia
§ Neoplastic, parasitic, hypereosinophilic syndrome
○ Neutrophilia
§ Toxic changes suggestive of infectious process
§ Left shift only non-specific - Diagnostic imaging
○ Radiography - best for assessing size
○ Ultrasound
§ Diffuse changes, focal masses, venous congestion (RSCHF), other abdominal organs, anomalous vessels
§ What looks like severe changes doesn’t always reflect histopathology
FNA cytology in investigation of liver disease risk, types in cat and what good for
○ Minimal risk (and sample size)
○ Guided or blind
§ Blind sites
□ Cat - right lateral recumbency and go on the left, fingers secure the liver towards the skin
® If do on the right then have a risk of getting gall bladder
○ Good for things that exfoliate:
§ Lymphoma, mastocytosis, amyloidosis, lipidosis, glycogen deposition, vaculoar hepatopathy
§ Therefore in cats with large smooth livers
Biopsy needle vs wedge for assessment of liver disease what need to consider
○ Is the lesion accessible percutaneously
○ Is owner/animal stable enough for surgery
○ Could surgery be therapeutic as well
○ Don’t waste the GA
○ Is lesion solitary or diffuse
§ Solitary lesions that can dissect -> surgery
○ Get lots of needle samples
○ MUST CHECK COAGULATOPATHY TIMES BEFORE THIS WHEN JAUNDICE
Acute hepatopathies cause and what results in most cases
In many cases the underlying aetiology CANNOT be identified until animal is stabilised
○ Generally cannot get liver biopsies anyway because of large coagulopathy
Causes
- Infectious (viral and bacterial)
- Toxins - food, mycotoxins, zamia pinenuts
- Drugs (paracetamol in cats, idiosyncratic)
- Others (GDV, DIC, pancreatitis, neoplasia)
Acute hepatopathies what reuslt in and clinical signs,diagnosis
- Hepatic necrosis
- +/- hepatocellular injury -> don’t learn the whole list - just know that hepatocytes are sick/damaged
Clinical signs and diagnosis - Sub-clinical -> acute onset lethargy, vomiting and jaundice -> encephalopathic crisis
○ VERY HIGH ALT/AST, lesser for ALP
○ Often abnormal clotting times
○ High bilirubin
○ Biopsies show various degrees of hepatic degeneration and necrosis
Acute hepatopathies prognosis when better, does liver enzyme increase count and what could progress to
- Better prognosis if known and can correct underlying cause
- The more severe the clinical signs the more aggressive the treatment needs to be
○ Survival not proportional to amount of liver enzyme increase - Could progress to fibrosis or cirrhosis or complete recovery
What are the 8 potential steps in the general treatment of hepatopathies depending on cause
1) correct acid-base and electrolyte abnormalities
2) control sepsis - systemic antibiotics
3) treat hepatic encephaopathy if concerned
4) control conrueent signs
5) avoid potentiating factors - don’t use medications metabolised by liver - barbiturates
6) paracetamol toxicity - N-acetycysteine (mucomyst), ascorbic acid, cimetidine
7) anti-oxidants
8) ursodeoxycholid acid - natural bile acid
when correcting acid-base and electrolyte abnormalities in acute hepatopathie what need to use and ensure doesn’t get
○ IV fluids: correct dehydration then 1.5 times maintenance unless also nephrotoxin
○ Ensure does not get hypokalaemia (will worsen hepatic encephalopathy)
○ Avoid alkalinising fluids > NOT HARTMANNS - makes hepatic encephalopathy worse)
If concerned about hepatic encephaopathy what need to give
○ Reduce circulating toxins
i. NPO 12-36 hours - fast the animals
ii. Cleansing enema -> reduce ammonia producing bacteria within colon
iii. IV antibiotics - if haven’t already
iv. Then retention enemas until no longer signs of hepatic encephalopathy
□ Oral Lactulose, vinegar - once able to take
What are 5 possible cocurrent signs with acute hepatopathie that need to control and how
○ Coagulopathy -> vitamin K ○ GI haemorrhage -> omeprazole ○ Cerebral oedema -> mannitol ○ Hypoglycaemia -< dextrose solution IV ○ Seizures -> gabapentin or propofol - NOT BARBITUATES
Anti-oxidants what is their role with acute hepatopathies and which use
○ Some role in acute hepatopathies such as paracetamol toxicity
§ Use vitamin E and C in this case NO OTHERS BECAUSE CAN OVERDOSE
What if you have a well dog with High ALP and very jaundice what thinking and causes
- Generally not hepatic or pre-hepatic because generally sick
- MOST COMMON ISSUE -> obstruction -> POST HEPATIC
- infection/inflammation
- Stasis
- Obstruction
• Choleliths
•Neoplasia
•External (pancreas, duodenum)
What are the 3 main things within the approach to figuring out if hepatic or post-hepatic jaundice and which best
1) Look at animal
○ Is it painful
○ Was it painful and now looks fine
§ Was there an abscess or mucocoeles that has rupture
2) Look at haemtology
3) Image the abdomen
○ X-ray somewhat useful, especially if sick and pyrexia
§ If have gas within liver -> surgical condition
○ Ultrasound very useful
§ If indicated take sample bile for culture
Gall bladder mucocoele how occurs, what often associated with, what are the 2 main outcomes
- Change in composition of bile so becomes inssiptaed +/- superimposed infection
- Often associated with underlying endocrinopathy
○ Hypothyroidism
○ Hyperadrenocorticism - Can be incidental finding OR surgical emergency
Gall bladder mucocoele when is it a surgical emergency - EXAM
§ Free abdominal fluid within bilirubin or bacteria within
§ Very sick, pyrexic animal (requires stabilisation first)
□ Exception is acute pancreatitis - virtually never surgical
§ Free gas on abdominal radiograph
§ Obvious mass or stone in biliary system on imaging
Idiopathic nodular hyperplasia how common in dogs, what forms nodules, is it an issue, what enzyme increases, what may also have and diganosis
LARGE LUMPY LIVER
- Very common and benign disease of older dogs
- Discrete accumulation of hyperplastic hepatocytes that form nodules
- Often incidental finding as asymptomatic
- Massively increased ALP (only)
- May have concurrent disease (hyperadrenocorticism)
- Diagnosis
○ Often appears nasty on ultrasound
○ Needle biopsies may not distinguish from adenomas
○ Need large wedge biopsy for definitive diagnosis
- DO NOT USE THIS DISEASE AS AN EXCUSE FOR SICK DOG
Liver neoplasia example of primary and metastatic, clinical signs, diagnosis and prognosis
LARGE LUMPY LIVER
- primary - adenoma, hepatocellular carcinoma
- metastatic - lymphoma
- non-specific clinical signs - liver failure, paraneoplastic sydnrome, asymmetric hepatomegaly
- Diagnosis - need large biopsy for diefinitive diagnosis - remove entire affected lobe
- prognosis - reasonable with entire excision
Vacuolar hepatopathies how common, why occur, what vacuoles contain and diagnosis
- Most common cause of smooth and large livers in dogs
- Liver reacting to other disease
- Vacuoles may contain
○ Lipid, glycogen or metabolic wastes - Diagnosis
○ Marked increase in ALP
○ Hyperechoic, diffuse, hepatomegaly
○ FNA often diagnostic
Vacuolar hepatopathies causes
○ Hyperadrenocorticism - MAIN CAUSE ○ Diabetes mellitus ○ Pancreatitis ○ Lipid metabolism disorders ○ Chronic stress ○ Severe hypothyroidism ○ Glucocorticoid administration
Chronic hepatitis list some causes, clinical signs, diagnostic appraoch
SMALL AND BUMPY LIVER - Many causes ○ Relapsing pancreatitis/IBD ○ Bile duct obstruction ○ Chronic toxin ingestion ○ Breed-related disorders 0 IMPORTANT ○ Auto-immune disease - Clinical signs ○ Similar despite differing causes § Malaise, jaundice, ascites through to liver failure - Diagnostic approach similar for all causes -> Rely on biopsy for more definitive diagnosis ○ Not always made ○ Need coagulation times before biopsy
Breed-specific hepatopathies what result in and diagnosis
CHRONIC HEPATITIS - small and bumpy liver
- Diagnosis
○ Present at any age (young-middle ages)
○ Clinical signs
§ Can wax and wane, polydipsia, weight loss, ascites, depression, vomiting and diarrhoea (melena and haematemesis)
§ Jaundice terminally
○ Biochemistry
§ Liver enzymes usually increase except terminally
§ May have evidence of decreased liver function
§ Imaging usually small liver with patchy echogenicity
§ Need biopsy-> Need coagulation testing BEFORE BIOPSY
What are the 4 main forms of breed-specific hepatopathies
1) Bedlington terriers and copper toxicosis
2) dalmatians, west highland white terriers
3) skye terriers
4) chronic active hepatitis -§ Self-perpetuating immune response with necrosis that -> cirrhosis
- Initiating factor unknown
Hepatic fibrosis main causes presentation, clinical signs and diagnosis
- Secondary to most cause chronic or acute hepatic disease
- Idiopathic hepatic fibrosis
○ Primary disease
○ Classified according to anatomical distribution
○ Uncommon
○ Young dogs (<2 yo)
○ Often concurrent portal veins defects
○ Clinical signs
§ Portal hypertension - multiple extra-hepatic shunts as trying to divert around high pressure area
§ Mild decrease liver function
§ +/- hepatic encephalopathy
§ Very rarely icteric
○ Small liver
○ US see secondary shunts
○ Liver biospy
○ Treat as for others
What are the 2 main steps in the treatment of chronic liver conditions
1) identifiy and treat initiating factor if known
- if copper most apparent - anti-copper medication
- if fibrosis most apparent - anti-fibrotic agents
2) medical management of decreased liver function if present
Identify and treat initiating factor if known for chronic liver conditions what are the 2 main things within a what can use
1) Anti-copper medications § Must confirm copper role § D-penicillamine □ Anti-collagen as well □ Ensure not too low Cu □ Divided doses § Zinc salts □ 3 months to reverse § Newer drug available - trientene 2) Anti-fibrotic agents § Fibrosis common consequence of many diseases § No specific drugs to counteract TGF-beta § SAMe, milk thistle, vit E § Prednisolone, azathiprine, pencillaemine and zinc
Medical management of decreased liver function if present in chronic liver condition what is involved
○ Diet modification as for HE ○ Treat GI ulceration ○ Manage coagulopathies ○ Manage HE ○ Treat ascites § Low-sodium diet § May reverse if treatment underlying disease § Spironolactone
Cats with liver disease what often also have and the 3 main causes of large smooth liver
often have pancreatic or intestinal disease
- inflammatory liver disease
- hepatic lipidosis
- neoplasia - lymphoma
Inflammator liver disease how common, how to differentiate the types and the main nes
- 2nd most common cause of feline liver disease (lymphoma is 1)
- Large overlap in signalment, clinical signs and clinicopathological changes
- Need biopsy/cytology to differentiate between type but biopsy not always necessary
- Types
○ Cholangohepatitis - now called cholangitis (CCH)
1. neutrophilic cholangitis (NC)
2. lymphocytic cholangitis (LC)
3. destruction cholangitis (DC)
4. chronic cholangitis (CC)
What is neurtophilic cholangitis , forms, what can see and presentation
Neutrophils in lumen and/or epithelium of bile ducts
□ Acute and chronic forms
® Chronic stage get mixed inflammation
® Due to ascending infection from GI tract
□ Can see bacteria using FISH
□ Usually sicker and younger
What is involved with lymphocytic cholangitis, cause, breed, what can look like
□ Infiltration of lymphocytes and plasma cells around portal areas with variable degrees of fibrosis and biliary hyperplasia
□ Immune-mediated onset and progressive
□ Persians over-represented
□ Leads to abdominal effusion - looks like FIP
□ Difficult to distinguish from lymphoma
What is involved with destruction cholangitis and chronic cholangitis and causes
1) Destruction cholangitis (DC)
□ Loss of bile ducts and fibrosis with inflammation and fibrosis
□ Idiosyncratic reaction to drugs/toxins as well as viral causes
2) Chronic cholangitis (CC)
□ Dilated larger bile ducts with papillary projections and fibrosis
□ Liver fluke infestation
Inflammatory liver disease in cats what 4 things use for diagnosis
1) biochemistry
2) imaging
3) cytology
4) biopsy
