Hepatology 3 Flashcards
- Purposes of diet modification in managing liver disease?
- Instances in liver disease where complication management may be needed?
- Other therapies in managing liver disease?
- To avoid exacerbating hepatic dysfunction.
+/- copper restriction. - Hepatic encephalopathy.
Portal hypertension. - Anti-inflammatory / immunosuppressive therapies.
Other specific therapies e.g. copper chelation, treatment of infectious agents, neoplastic disease (chemo).
Hepatoprotective therapies - antioxidants, choleretics (facilitate bile flow).
Various supportive therapies - fluids, nutrition, anti-emetics.
Main cause of ammonium biurate crystals on urinalysis sediment examination.
liver dysfunction
What if bloods show extreme hepatic dysfunction with fairly normal liver enzymes?
Extreme hepatic dysfunction due to inadequate blood supply or vascular aberrancy to liver, and therefore dysfunction due to shunting of blood (liver cells themselves are heathy, just have fewer of them and not getting the blood supply they should be),
OR
Got such end-stage liver disease that there is very little cells to produce enzymes anymore.
*Imaging helpful for detecting which one.
Differentiation between congenital and acquired portosystemic shunting?
Congenital = one abnormal vessel.
Acquired = lots of small abnormal vessels.
Age.
Clinical problems in congenital PSS patients.
Hepatic encephalopathy.
Inappetence.
GI signs - V+/D+.
Lower UT signs.
- urolithiasis – ammonium biurate.
- UT infections – poor immunity.
Coagulopathies / GI haemorrhage (upper GI ulcers in intrahepatic shunts).
Signs characteristically wax and wane.
Usually signs present since birth.
Congenital PSS management.
Surgical:
- normalise macroscopic vascular anatomy to prevent further shunting.
- requires period of pre-operative medical stabilisation.
- generally, better long-term outcome – at the very least all patients should be offered a specialist consultation.
Medical:
- as a precursor to intended surgical treatment – star pending referral.
- as a long-term option where surgery declined / not possible.
Medical therapy for hepatic encephalopathy at home?
Dietary modification:
- protein modification to minimise encephalopathy.
- vegetable based protein vs protein restriction.
– meat protein more likely to be metabolised to aromatic amino acids which are encephalopathic.
- +/- cottage cheese.
Lactulose:
- titrate dose to avoid laxative effects.
- disaccharide – colonic bacterial fermentation –> SCFAs.
- ion traps ammonia in colon
– NH3 –> NH4+.
ABX - rarely indicated.
Hepatic encephalopathy crisis management in PSS patients.
As per standard HE management.
PLUS…
Ensure euhydrated, normokalaemic with IV fluids.
Precipitating factor?
- address fluid losses (urinary, GI).
- dietary/protein modification / GI haemorrhage.
Lactulose retention enema.
Check blood glucose.
Anti-epileptic therapy:
- Levetiracetam vs. phenobarbitone.
Mannitol? - controls cerebral oedema.
Other medical considerations for PSS patients?
Inappetence - palatability considerations vs medical management.
Can give appetite stimulants and
GI signs - avoid fluid deficit.
Lower UT signs:
- urolithiasis – may dissolve post-op / may need intervention / surgery.
- UTIs – ABX indicated.
Coagulopathies / GI haemorrhage:
- check coagulation times (PT/aPTT).
- gastric ulceration/haemorrhage esp. in intrahepatic shunts.
– look for evidence e.g. melena or look at haematology to find regenerative anaemia.
– would benefit from acid blockers e.g. omeprazole.
- What are the most common bacteria causing cholangitis/cholangiohepatitis in cats and dogs?
- Most appropriate empirical treatment for cholangitis/cholangiohepatitis?
- E. coli.
Enterococcus. - Amoxicillin/clavulanic acid.
Marbofloxacin if resistance to amoxicillin.
Enrofloxacin in cats causes retinal detachment.
Other times when specific antibiotic use may be indicated in liver disease.
When suspect/confirm leptospirosis.
- amoxicillin-clavulanate / penicillins – IV / pending results
- doxycycline – 2 weeks oral to clear carrier state.
Hepatic abscess.
- Sx and ABX (empiric e.g. amoxicillin-clavulanate, then guided by C&S).
Toxoplasmosis (cats, uncommon).
- Clindamycin, others.
- Protozoa – some antimicrobials have efficacy.
Choleretics.
Stimulate bile flow.
Ursodeoxycholic acid (UDCA).
- trade name Destolit.
Hydrophilic, ‘beneficial’ bile acid.
- attract water and increase bile fluidity.
Synthetically derived.
Mechanism:
- alters bile composition.
- modulates inflammatory responses in the liver.
- modifies immune response and minimises apoptosis.
- works to some degree as an antioxidant.
Little evidence for its use.
Indicated for:
- cholestatic disease e.g. as adjunct in biliary disease e.g. cholangitis, gall bladder mucocoele).
Not safe for use in rabbits.
Antioxidants.
N-acetyl-cysteine (IV option).
- extreme toxic insult.
Milk thistle extracts / isolates.
- Silymarin / silibinin / sylibin / silybum.
S-adenosyl-L-methionine (SAMe).
Vitamin E - poor evidence.
Vitamin C? - poor evidence.
S-adenosyl-L-methionine (SAMe).
Natural antioxidant that is produced in liver from methionine by enzyme SAMe synthetase.
Liver should produce plenty of this when healthy
But liver cannot produce very much of this when it is diseased.
SAMe is a precursor for cysteine which is one of the components of glutathione which is an antioxidant.
Proven to be effective in mushroom toxicity
But useful in the chronic setting too.
Trade names = Samylin, Denamarin, Zentonil.
Anti-inflammatories / immunosuppressives.
Steroids (prednisolone).
- anti-inflammatory vs immunosuppressive.
- E.g. chronic hepatitis (some cases), lymphocytic cholangitis.
Immunosuppression:
- Diseases benefitting from immunosuppression:
– lymphocytic cholangitis.
– chronic hepatitis?
- Start with steroids.
- May need adjuncts e.g. chlorambucil for cats.
