Hepatobiliary 1 Flashcards

1
Q

when loss of 60-80% functional hepatic tissue occurs, ___________ results

A

hepatic failure
(occurs late in disease)

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2
Q

what are at least 5 signs of hepatic failure

A

decreased appetite, vomiting, lethargy, weight loss, icterus, hepatic encelopathy, abdominal effusion and/or pain, micro hepatica or hepatomegaly, fever (if infectious or bile peritonitis)

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3
Q

name bloodwork findings for: pre-hepatic disease

A

pale and icteric
anemia

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4
Q

name bloodwork and US findings for: hepatic disease

A

normal PCVC, elevated liver enzymes (ALT due to hepatocellular injury), no evidence of post-hepatic obstruction on US

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5
Q

name bloodwork and US findings for: post-hepatic disease

A

normal PCV, elevated liver enzymes (ALP, bili, GGT (cholestatic indicators)
post-hepatic obstruction on US

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6
Q

what is hepatic encelopathy?

A

NEUROLOGICAL signs arising from liver dysfunction due to accumulation of toxic byproducts (proposed toxins include AMMONIA , aromatic AAs, false NTs); the toxins accumulate due to altered hepatic clearance and metabolism

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7
Q

hepatic enceloppathy common therapies target decreasing _____ concentrations

A

ammonia

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8
Q

cat presents with intermittent signs of confusion, dull behaviour, head pressing, seizures and hypersalivation; these seem to be associated around mealtimes. what is your suspicion based on these C/S?

A

hepatic encelopathy
(mild presentation; acute severe presentation would be coma, recumbency, death)
note cats hyper salivate, not dogs

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9
Q

what are 3 most common HE-associated conditions in cats?

A

diversion of portal blood flow (congenital shunting), fulminant acute hepatic necrosis, and hepatic lipidosis

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10
Q

what are 3 most common HE-associated conditions in dogs?

A

diversion of portal blood flow (congenital shunting), fulminant acute hepatic necrosis, and reduction in hepatic mass with diversion of portal flow (acquired shunting)

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11
Q

how is HE treated

A
  • Abx: neomycin, metronidazole, amoxicillin
  • lactulose to trap ammonia, PO or PR
  • reduced protein diet, as much protein as tolerated
  • if severely affected patients: hospitalize, decrease colonic bacteria with cleansing enemas
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12
Q

HE treatment: what 2 things are not synthesized as much with HE

A

serum proteins (albumin, tpt proteins) and glycogen storage/glucose synthesis are decreased in advanced hepatic disease

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13
Q

ethologies of ascites

A

main: portal hypertension -> collagen deposition -> disorganization of parenchyma and interruption of vasculature -> increased hydrostatic pressure and acquired shunts
minor: hypoalbiminemia
note, not commonly seen in liver disease cats

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14
Q

fat cat was left several days without food and now is vomiting, inappetent, lethargic, dehydrated, icteric, and has palpable liver margins. what is wrong

A

likely hepatic lipidosis

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15
Q

what bloodwork and urine findings would you expect with hepatic lipidosis

A

bili, ALP increased, ALT moderate increase, but GGT NORMAL (or mild increase)
bilurubinuria
high albumin (dehydrated)
no inflammatory leukogram, no elevated globulins, and no fever

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16
Q

cat AUS shows hyper echoic parenchyma and hepatomegaly. cytologyy shows >80% of hepatocytes infiltrated with lipid. what is going on? do you need a biopsy to confirm

A

supportive dx for hepatic lipidosis. often is a presumptive dx based on lab findings, +/- cytology, and response to tx

don’‘t biopsy. liver is fragile and can bleed

17
Q

tx for hepatic lipidosis

A

food!!!!: high calorie high protein, not protein restricted
start at 25 RER then increase daily to full RER
NE then esophageal or gastric tube (coat testing prior, via K)
fluid therapy with normosol, .9% saline, or plasmalyte A; monitor for hypophos and hypokalemia
antiemetics (Cerenia, metoclopramide which is also pro kinetic)

18
Q

secondary therapies for tx of hepatic lipidosis

A

Sam-e, ursodiol, carnitine, taurine; most important is tx of primary dz if identified

19
Q

liver disease in cats: what are 3 components of triaditis

A

cholangitis, pancreatitis, inflammatory bowel dz

20
Q

what is neutrophilic cholangitis

A

neutrophils in bile duct lumen and epithelium; can extend into parenchyma; due to ascending infection from GIT? ; can be classified as acute or chronic

21
Q

compare and contrast neutrophilic and lymphocytic cholangitis: signalment and history

A

neutrophilic: middle aged to older cats, typically acute presentation
lymphocytic: young cats mostly, Persian breed

22
Q

compare and contrast neutrophilic and lymphocytic cholangitis: C/S and clin path findings

A

neutrophilic: febrile, anorexia, lethargy, pyrexia, icteric, vomiting
neutrophilic leukocytosis, elevated hepatic enzymes

lymphocytic: icterus, afebrile, hyperglobulinemia, elevated liver enzymes and bilirubin, +/- ascites and enlarged mesenteric LNs, abdominal distension possible, abdominal fluid is often yellow tinged with high protein content

23
Q

what is required for definitive diagnosis of neutrophilic or lymphocytic cholangitis

A

liver biopsy cuture and histopath

also you should do HI and pancreas histopath plus bile cytology and culture bc liver sample will take awhile to process

24
Q

how to treat neutrophilic cholangitis

A

Abx based on C&S; Clavamox good initially, 6-8 weeks
fluids and antiemetics
hepatic support: ursodiol, same-E
enteral nutrition if anorexic

25
Q

what is etiology of lymphocytic cholangitis

A

unknown, immune mechanism suspected

26
Q

how to treat lymphocytic cholangitis

A

corticosteroids: prednisolone 1-2 mg/kg q12h PO; taper to LED
supportive care: ursodiol, sam-e, enteral nutrition if anorexic

27
Q

you perform PE, CBC chem, urinalysis due to suspicion of hepatic lipidosis. findings are supportive. are you considering any other additional tests?

A

PT/PTT - need to perform clotting tests prior to a biopsy
FeLk/FIV in case of contact w other cats
AUS for comorbidities and to assess liver

28
Q

what is the most common hepatobiliary congenital anomaly

A

portosystemic shunt (this is direct venous communication between portal vein and systemic circulation, ie. bypassing liver)

29
Q

describe typical signalment of PSS

A

1-2 years, any breed dog: small breed yorkies, Maltese, cairn terrier, pug, extrahepatic most common; large breed intrahepatic most common; cats less common, get extrahepatic

30
Q

young dog growing poorly, poor recovery under anesthesia, PUPD, HE, and (30% have) urinary tract signs. blood: microcytosis, hypoalbuminemia, low BUN, ALT and ALP (may have) mildly elevated. what might be going on?

A

PSS

31
Q

what are UA findings with PSS

A

low. USG: over 50% hyposthenuric or isisthenuric
ammonium bitrate crystals: 50% dogs, 15% cats

32
Q

besides bloodwork, UA, what are other diagnostic findings with PSS

A

increased ammonia levels: Se but not done in clinical practice
increase bile acids: Se
abdominal rads: micro hepatica common, bilateral renomegaly,ammonium bitrate calculi but these don’t show on rads

33
Q

how is definitive dx of PSS made

A

US, direct visualization, CT are preferred

34
Q

what are some concurrent defects that occur w PSS

A

cryptorchid
heart our jr
Cu colorez irises cats

35
Q

prior to definitive sx therapy, what do you need to do for PSS patients

A

stabilize them
treat HE
pre-op anti-epileptic meds may be recommended

36
Q

what is portal vein hypoplasia

A

microscopic anomaly of portal veins; abnormal connections between portal veins and systemic circulation at microscopic level; con occur concurrently with PSS

37
Q

what breeds are predisposed to macroscopic shunts

A

same as with PSS (Maltese, Pug, small breed Yorkies, Cairn Terrier); latter 2 overrepresented

38
Q

what are the 2 clin pres of PVH

A

asymptomatic
symptomatic: C/S develop later in life than PSS; mild GI signs or signs of HE possible; will be milder than with PSS

39
Q

what is tx for PVH

A

supportive: treat HE if present; consider hepatic supportive therapies (Same-e)
rule out other vascular abnormalities; may have concurrent PSS
no sx therapy