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Small Animal Medicine: Exam 2 (Spring 2016) > L19: Management Of Liver Disease (Hill) > Flashcards

L19: Management Of Liver Disease (Hill) Flashcards

1
Q

Which breeds prone to extrahepatic congenital PSS?

A

Lhasa
Shih Tsu
Schnauzer
Yorkie

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2
Q

Which breeds prone to intrahepatic congenital PSS?

A

Irish wolfhound
Irish Setter
Labs

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3
Q

Which breeds prone to microvascular dysplasia?

A

Yorkies

Cairn terriers

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4
Q

Congenital hepatic vascular abnormalities

A

Extrahepatic PSS
Intrahepatic PSS
Microvascular dysplasia (many small shunts)
AV fistula

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5
Q

Tx of PSS

A

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
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6
Q

Common liver toxins that cause ACUTE to FULMINANT hepatic necrosis

A
  • acetaminophen
  • caparsolate (old heartworm tx)
  • blue green algae
  • sago palm
  • moldy food
  • amanita mushrooms

*prognosis poor with fulminant necrosis

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7
Q

Common liver toxins that cause CHRONIC hepatic changes

A
  • oxibendazole and DEC
  • Carprofen
  • Phenobarb
  • Primidone
  • phenytoin
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8
Q

Acute tx of toxin exposure

A
  • if hypoxic, restore airway, breathing, circulation
  • remove toxin (ie. Dialysis)
  • give antidote/tx for specific toxins
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9
Q

Antidote to amanita poisoning

A

Sylimarin

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10
Q

Antidote to acetaminophen toxin

A

Acetyl cysteine

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11
Q

Tx of copper and iron toxicity

A
  • penicillamine
  • trientene
  • Zinc (inhibits Cu absorption)
  • Cu restricted diet (l/d
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12
Q

CS of Cu deficiency

A

Similar to Fe deficiency anemia

-also: cardiac dz, low WBCs

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13
Q

Forms of hepatic lipidosis in cats

A
  • idiopathic (most common)

- secondary (2ary to DM, hypothyroidism, pancreatitis/triaditis)

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14
Q

Tx of hepatic lipidosis in cats

A
  • 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
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15
Q

Forms of infectious hepatitis

A
  • viral
  • bacterial
  • protozoal
  • fungal
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16
Q

3 viral hepatitidies

A

CAV-1
Acidophil cell hepatitis
FIP

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17
Q

Bacterial hepatitidies (and tx)

A

Lepto: penicillin, doxy
Bartonella: enrofloxacin, doxy, azythromycin

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18
Q

Protozoal hepatitidies and tx

A

Leishmania: allopurinol
Toxoplasma: TMS, pyrimethamine
Hepatozoon: Imidocarb

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19
Q

Clinical approach to liver flukes

A

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
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20
Q

Clinical approach to cholecystitis

A
  • 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
21
Q

Clinical approach to Feline cholangiohepatitis

A
  • 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
22
Q

Ursodeoxycholic acid (ursodiol)

A
  • 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
23
Q

Surgical biliary diseases

A
  • 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

24
Q

Primary hepatic neoplasia

A

Hepatoma
Bile duct carcinoma
Tx: sx, since has poor response to chemo (P glycoprotein) - liver naturally gets rid of chemo

25
Q

Top 3 metastatic hepatic neoplasms

A

LSA
HSA
MCT

26
Q

Breed disposition of idiopathic chronic hepatitis

A

Doberman
Cocker spaniel
Westies

27
Q

Etiology of idiopathic chronic hepatitis

A

Unknown (possibly immune-mediated)

28
Q

Dx of idiopathic chronic hepatitis

A

Biopsy showing bridging necrosis, lymphocytic-plasmacytic infiltration progressing to cirrhosis

Very guarded prognosis

29
Q

Tx of idiopathic chronic hepatitis

A

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

30
Q

Colchicine

A
  • microtubule inhibitor for idiopathic chronic hepatitis
  • inhibits collagen deposition, stimulates collagenase, may decrease inflammation
  • no objective data to support efficacy
31
Q

Sylimarin (milk thistle) for idiopathic chronic hepatitis

A
  • antioxidant, leukotriene, and TNF inhibitor
  • inhibits P glycoprotein and P450 enzymes
  • uncertain efficacy/dose
32
Q

Supportive therapy for idiopathic chronic hepatitis

A

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)

33
Q

Nutrition for tx of idiopathic chronic hepatitis

A
  • high protein (unless has PSS or chronic cirrhosis)
  • folate, B12, SAMe for methyl transfer
  • Choline for phospholipid export
  • Vitamin K for bile obstruction
34
Q

Oxidation important mech. For continued damage in cholestatic and other liver diseases due to:

A

Divalent cations, kupfer cells, bile acids

Prevent with Vitamin E and C

35
Q

Too much Vitamin E can –>

A

Inhibit Vitamin D and K absorption

36
Q

Methyl transfer cycle, and how affected by liver failure

A

Methionine –> SAMe –> S-adenosyl Homocysteine –> Homocysteine –> Methionine

*liver failure prevents methionine –> SAMe
(So may need to supplement SAMe in liver failure patients)

37
Q

Liver damage reduces methylation reactions which synthesize:

A
  • nucleic acids and amino acides
  • phosphatidylcholine
  • polyamines and GSH
38
Q

Denosyl =

A

SAME

-give 1 hr. Before feeding

39
Q

Symptomatic therapy of idiopathic chronic hepatitis

A
  • appetite stimulants
  • antiemetics
  • mucosal protection
  • Rx for hepatic encephalopathy and/or ascites**
40
Q

Causes of neurological signs

A
  • 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
41
Q

Tx of hypokalemic acidosis

A

Give potassium

42
Q

Sources of protein (and urea) in the large intestine

A
  • indigestible protein in the diet

- blood from gastric ulceration

43
Q

Prevention of protein in the large intestine

A
  • 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
44
Q

Etiology of hepatic encephalopathy

A
  • tryptophan is precursor for false NT

- competition for BBB transporter by branched chain aa

45
Q

Prevention of hepatic encephalopathy

A
  • Plasma: albumin binds tryptophan

- increased branched chain aa and decreased aromatic aa including Tryptophan

46
Q

Tx of hepatic encephalopathy

A

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

47
Q

Tx of ascites

A
  • 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
48
Q

Summary points

A
  • 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
49
Q

Management of liver dz: assessment before tx:

A

CBC, Chem, UA, function tests, imaging, biopsy

Small Animal Medicine: Exam 2 (Spring 2016) (13 decks)

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