L19: Management Of Liver Disease (Hill) Flashcards
Which breeds prone to extrahepatic congenital PSS?
Lhasa
Shih Tsu
Schnauzer
Yorkie
Which breeds prone to intrahepatic congenital PSS?
Irish wolfhound
Irish Setter
Labs
Which breeds prone to microvascular dysplasia?
Yorkies
Cairn terriers
Congenital hepatic vascular abnormalities
Extrahepatic PSS
Intrahepatic PSS
Microvascular dysplasia (many small shunts)
AV fistula
Tx of PSS
Ligation or coil for shunt if congenital with no portal hypertension
- 6% die with sx
- use keppra to prevent seizuring
- sx should be considered if bile acids are increased, which is an indication that treating the shunt will give the dog more functional liver
Common liver toxins that cause ACUTE to FULMINANT hepatic necrosis
- acetaminophen
- caparsolate (old heartworm tx)
- blue green algae
- sago palm
- moldy food
- amanita mushrooms
*prognosis poor with fulminant necrosis
Common liver toxins that cause CHRONIC hepatic changes
- oxibendazole and DEC
- Carprofen
- Phenobarb
- Primidone
- phenytoin
Acute tx of toxin exposure
- if hypoxic, restore airway, breathing, circulation
- remove toxin (ie. Dialysis)
- give antidote/tx for specific toxins
Antidote to amanita poisoning
Sylimarin
Antidote to acetaminophen toxin
Acetyl cysteine
Tx of copper and iron toxicity
- penicillamine
- trientene
- Zinc (inhibits Cu absorption)
- Cu restricted diet (l/d
CS of Cu deficiency
Similar to Fe deficiency anemia
-also: cardiac dz, low WBCs
Forms of hepatic lipidosis in cats
- idiopathic (most common)
- secondary (2ary to DM, hypothyroidism, pancreatitis/triaditis)
Tx of hepatic lipidosis in cats
- tx underlying cause (ie. IBD)
- E-tube and introduce high protein, high fat food slowly (high protein helps export fat from liver)
- monitor for refeeding syndrome (excess glucose goes to liver and gets converted to fat)
- tx atypical cushings with melatonin and/or lysodren in diet
Forms of infectious hepatitis
- viral
- bacterial
- protozoal
- fungal
3 viral hepatitidies
CAV-1
Acidophil cell hepatitis
FIP
Bacterial hepatitidies (and tx)
Lepto: penicillin, doxy
Bartonella: enrofloxacin, doxy, azythromycin
Protozoal hepatitidies and tx
Leishmania: allopurinol
Toxoplasma: TMS, pyrimethamine
Hepatozoon: Imidocarb
Clinical approach to liver flukes
Platynosomum concinnum
- causes bile duct obstruction, pancreatitis, chronic liver dz
- can cause acute AND chronic disease
- tx: high dose praziquantel
- may or may not get quick resolution w/ tx
Clinical approach to cholecystitis
- caused by ascending or systemic infection (usually E. Coli)
- usually a benign finding
- choleliths are less common cause
- tx: abx and supportive care if milder, cholecystectomy if severe
- prognosis guarded to poor
Clinical approach to Feline cholangiohepatitis
- usually caused by anaerobes and Gram - bacteria ascending from biliary tree
- GB can leak and cause bile peritonitis
- Dx by biopsy and culture
- can be suppurative (neuts) or non-suppurative (lymphs)
- Tx: abx (clavamox) +/- prednisone if non-suppurative over 3-4+ months
Ursodeoxycholic acid (ursodiol)
- hydrophobic bile acid that displaces endogenous hydrophobic bile acids that accumulate in cholestatic dz
- anti-inflammatory, increases bile flow
- originally from bears
- contraindicated if complete obstruction
- very expensive
Surgical biliary diseases
- biliary obstruction: tumor, gall stones
- Emphysematous cholecystitis
- Mucocele
*very guarded prognosis (7-50% mortality rate), since by the time we remove GB it is very diseased
Primary hepatic neoplasia
Hepatoma
Bile duct carcinoma
Tx: sx, since has poor response to chemo (P glycoprotein) - liver naturally gets rid of chemo
Top 3 metastatic hepatic neoplasms
LSA
HSA
MCT
Breed disposition of idiopathic chronic hepatitis
Doberman
Cocker spaniel
Westies
Etiology of idiopathic chronic hepatitis
Unknown (possibly immune-mediated)
Dx of idiopathic chronic hepatitis
Biopsy showing bridging necrosis, lymphocytic-plasmacytic infiltration progressing to cirrhosis
Very guarded prognosis
Tx of idiopathic chronic hepatitis
1) Immunosuppressive therapy:
-prednisolone/budesonide (mineralocorticoids)
-Dexamethazone if have ascites
+/- azathioprine
prednisolone better than prednisone
2) Antifibrotic therapy: Colchicine
3) Herbal remedy: Sylimarin (milk thistle)
4) Supportive therapy
Colchicine
- microtubule inhibitor for idiopathic chronic hepatitis
- inhibits collagen deposition, stimulates collagenase, may decrease inflammation
- no objective data to support efficacy
Sylimarin (milk thistle) for idiopathic chronic hepatitis
- antioxidant, leukotriene, and TNF inhibitor
- inhibits P glycoprotein and P450 enzymes
- uncertain efficacy/dose
Supportive therapy for idiopathic chronic hepatitis
Fluids: glucose, no lactate (met. In the liver)
Plasma (binds amino acids and things that get transformed into neurotransmitters)
Nutrition
Antioxidants (Vit. E)
S-adenosyl methionine (SAMe)
Nutrition for tx of idiopathic chronic hepatitis
- high protein (unless has PSS or chronic cirrhosis)
- folate, B12, SAMe for methyl transfer
- Choline for phospholipid export
- Vitamin K for bile obstruction
Oxidation important mech. For continued damage in cholestatic and other liver diseases due to:
Divalent cations, kupfer cells, bile acids
Prevent with Vitamin E and C
Too much Vitamin E can –>
Inhibit Vitamin D and K absorption
Methyl transfer cycle, and how affected by liver failure
Methionine –> SAMe –> S-adenosyl Homocysteine –> Homocysteine –> Methionine
*liver failure prevents methionine –> SAMe
(So may need to supplement SAMe in liver failure patients)
Liver damage reduces methylation reactions which synthesize:
- nucleic acids and amino acides
- phosphatidylcholine
- polyamines and GSH
Denosyl =
SAME
-give 1 hr. Before feeding
Symptomatic therapy of idiopathic chronic hepatitis
- appetite stimulants
- antiemetics
- mucosal protection
- Rx for hepatic encephalopathy and/or ascites**
Causes of neurological signs
- ammonia from colon and kidney
- inhibitory GABA receptor stimulation of endogenous benzodiazepine ligands (benzos, barbiturates)
- false neurotransmitters
- methionine/mercaptons
- hypoglycemia (tx first)
- cerebral edema (tx w/ mannitol)
- hypokalemic alkalosis (K trapped intracellularly)
- dehydration
Tx of hypokalemic acidosis
Give potassium
Sources of protein (and urea) in the large intestine
- indigestible protein in the diet
- blood from gastric ulceration
Prevention of protein in the large intestine
- decrease protein in diet
- use digestible protein with good balance (ie. Egg, mixed protein, cottage cheese, veggie protein)
- avoid meat protein
- give mucosal protectants or antacids
Etiology of hepatic encephalopathy
- tryptophan is precursor for false NT
- competition for BBB transporter by branched chain aa
Prevention of hepatic encephalopathy
- Plasma: albumin binds tryptophan
- increased branched chain aa and decreased aromatic aa including Tryptophan
Tx of hepatic encephalopathy
Lower the pH and ammonia absorption by increasing bacterial fermentation of undigested carbs in LI:
- give lactulose +/- neomycin OR:
- metronidazole, rifaximin
- soluble fiber
Absorption: Metronidazole > Neomycin > Rifaximin
Tx of ascites
- plasma
- salt restriction
- spironolactone (aldosterone antagonist) +/- loop diuretic (furosemide) initially only
- paracentesis (ONLY for relief of breathing; can dehydrate patient quickly)
- abx if culture positive
- avoid liquorice-containing chinese meds
Summary points
- liver enzymes can decrease over time despite dz progression
- bile acids/ammonia don’t correlate well with function or signs
- Glu/Alb/BUN/PT/bilirubin affected LATE in liver dz
- bilirubin delta persists despite clinical improvement
Management of liver dz: assessment before tx:
CBC, Chem, UA, function tests, imaging, biopsy
