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Certifying Examination > Hepatobiliar > Flashcards

Hepatobiliar Flashcards

1
Q

Which reaction catalizes ALT?

A

Alanine + ketoroglutorate –> glutamate + pyruvate

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2
Q

Which reaction catalizes AST?

A

Aspartate + ketoroglutorate –> glutamate + oxaloacetat

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3
Q

Which toxins supress hepatic enzymes synthesis?

A

Microcistin and Aflatoxin B1

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4
Q

How many days G-ALP transcription is delayed after beginning exogenous corticoisteroids administration?

A

10d

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5
Q

Which are the causes of hyperammonemia?

A
  • PSS
  • Fulminant hepatic failure
  • Urea cycle defect:
    —- Transitory (Irish Wolfhounds puppies)
    —- Enzimatic deficiency (cats: ornithine transcarbamylase)
    —- Arginine deficiency (cats)
    —- Cobalamin deficiency
  • Urinary tract disease
  • L asparginasa treatment
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6
Q

Which molecules can produce hepatic encephalopathy?

A

Ammonia, GABA, endogenous benzodiazepines, glutamat, tryptophan, aromatic aa, bile acids, short chain fatty acids, phenol, decreased alfa ketoroglutorate, false neurotransmitters

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7
Q

Which primary hepatic diseases can have normal or mildly increases of hepatic enzymes?

A
  • Vascular disorders
  • End stage cyrrhosis
  • Metastatic hepatic neoplasia
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8
Q

Which hepatic disease produce the largest ALT increases?

A

Hepatocellular necro-inflammatory diseases

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9
Q

Which is the bile acid interpretation?

A
  • Pre<post: PSS, parenchymal hepatic disease, cholestatic disease
  • Pre>post: interdigestive gallbladder contraction, variations in gastric emptying/intestinal transit/response to CCK
  • False positives: glucocorticoids treatment, GI disease, phenobarbital treatment, seizures, tracheal collapse, lipemia
  • False negatives: no CCK production due to inadequate food, malabsorptive/maldigestive disease
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10
Q

Which renal disease can be secondary to Cu hepatopathy?

A

Fanconi like syndrome

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11
Q

Which extrahepatic disease is most associated with portal thrombus?

A

Pancreatitis

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12
Q

When are biopsies reccommended to be repeated once immunosupression/antiCu treatment have been started?

A
  • Cu hepatitis: 6m after starting Cu chelation tt
  • Chronic hepatitis (immunemediated?): 6w after steroids treatment
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13
Q

Which factors precipitate HE?

A
  • Dehydration
  • Increased protein ingestion
  • Hypokalemia
  • Alkalosis (acidosis?)
  • Infection
  • Sedatives/analgesics
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14
Q

Which is the classification of vascular hepatic disorders?

A

ACQUIRED
- MAPSS: secondary to portal hypertension

CONGENITAL:
- Macrovascular = PSS
—- IHPSS (25%)
—- EHPSS (75%)
- Microvascular = Portal Vein Hypoplasia
—- Without portal hypertension: Microvascular dysplasia
——– Primary
——– Associated with PSS (+ frec)
—- With portal hypertension: Non cyrrhotic portal hypertension

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15
Q

Which are the mechanisms by which vascular diseases can damage the system?

A
  • Accumulation of endogenous and exogenous toxins –> EH
  • Reduced blood flow to the liver –> failure of normal hepatic function
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16
Q

Which are the causes of mycrocitosis in PSS?

A
  • Defective iron transport mechanism
  • Decreased serum iron concentrations
  • Decreased total iron bindings capacity
  • Increased hepatic iron stores in Kuppfer cells
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17
Q

Which is the sensibility of BA for PSS?

A

Almost 100%

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18
Q

Which is the interpretation of rectal scintigraphy in vascular hepatopathies?

A

The radioisotope is administered rectally and the patient is evaluated by a gamma camera.
Rectal –> portal vein –> liver –> systemic circulation.

If there is a shunt, the radioisotope reaches the heart bypassing the liver –> calculation of percentage of portal blood bypassing the liver:
- <15% = normal
- >60-80% = PSS (cannot be distinguished IHPSS or EHPSS)
In PVH the scintigraphy usually is normal.

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19
Q

Which are the imaging tests for diagnosing PSS?

A
  • Ultrasound
  • CT
  • Scintigraphy
  • POrtography
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20
Q

Which is the mechanism of action of lactulose as a HE treatment?

A
  • Reduce transit time –>
    —- reduce time for bacteria to proliferate and produce ammonia
    —- eliminating bacteria and ammonium by feces
  • Colonic acidification –>
    —- trapping ammonia in the form of ammonium
    —- reducing the bacteria numbers
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21
Q

Which clinicopathological parameters can improve only with medical treatment?

A

ALT and ALP levels can be reduced (but not normalize). All the other clinicopathological alterations are mantained equal as previous medical treatment.

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22
Q

Which are markers of favorable response to medical treatment?

A

Age at onset of clinical signs (+ age, + prognosis)
Urea (+urea, + prohnosis)
The other alterations are not related with response.

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23
Q

Which is the prognosis of dogs with PSS and treated surgically?

A

PSS cannot be acutely closed due to portal hypertension development, as well as if not completely closed, 50% develop clinical signs months/yeard later.

  • EHPSS: 10-20% complications, exit rate ~85%
  • IHPSS: 50% complications, lower exit rate depending of the material (but more mantain a chronic communication)
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24
Q

Which are the potential causes of GI ulceration in PSS?

A
  • Hypergastrinemia
  • Hypoprostaglandinemia
  • Poor mucosal integrity
  • Abnormal mucus production
  • Abnormal cell turnover
  • Reduced blood flow
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25
Q

Which tests could serve as non invasive biomarkers of PSS closure?

A
  • Lidocaine and monoethylglycylxylidide (lidocaine metabolit): increase in closed PSS
  • Ratio branched/aromatic aa: increase in closed PSS
  • Serum hyaluronic acid: reduce in close PSS (specific marker for PSS)
  • IGF1: increase in closed PSS
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26
Q

Which special stains are used for glycogen and fat liver evaluation?

A
  • Glycogen: PAS
  • Fat: red oil
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27
Q

Which is the most common zone of glycogen deposition?

A

Zone 3

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28
Q

How is the vacuolization of a hepatic lipidosis?

A

A mixture of microvesicular and macrovesicular (DM is microvesicular)

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29
Q

Which are the main laboratorial abnormalities in a cat with feline lipidosis?

A
  • Increase triglycerids (but onw study discard that) and non-esterified FA
  • Increased LDL and reduced HDL
  • Increase BOHbutirate
  • Normal/reduced insulin –> no insulin resistant
  • Increased leptin (+ leptin resistance) and adiponectin
  • Reduced apoproteins (due to protein deficiency, specially taurine and carnitine)
  • Hyperglicemia
  • Hypokalemia
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30
Q

Which are new potential drugs for the treatment of feline lipidosis?

A
  • T863: diacilglicerol O-acetiltransferasa 1 (DGAT1) inhibitor (DGAT1 is the main enzyme responsible of the triacilglycerol synthesis)
  • AICAR: adenosine monophosphate kinase activator –> reduce fat levels reducing the expression of the enzyme PLIN2
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31
Q

Which prevalence of dogs with hepatocutaneous syndrome present with DM?

A

25-40%

32
Q

Which plasmatic and urinary markers can be used for ACHES?

A
  • Plasmatic: low 1-methylhistidine and cystathionine
  • Urinary: high lysine and mtehionine
33
Q

Which is the prevalence of dogs with ACHES that develops cutaneous signs?

A

75% –> hepatopathy seems to be an early step of the disease, and cutaneous signs a more delayed

34
Q

Which is the only lyososomal disease that affects primarily in the hepatic system?

A

Cholesterol ester storage disease (Fox Terriers)
Most lysosomal disease affects the neurologic/muscular system

35
Q

With which other mineral is associated Cu in liver?

A

With Pb (+Cu, +Pb)
And Pb associated with mycrocitosis

36
Q

Which breeds are predisposed to lobublar dissectans hepatitis?

A

Cocker Spaniel and Poodle

37
Q

Which is the prevalence of splacnic and portal thrombosis in dogs with chronic hepatitis?

A

~6%

38
Q

Which are the most common stains used for liver evaluation?

A
  • H&E
  • Rhodamine/rubeanic acid: Cu
  • Masson’s trichrome: fibrosis (collagen)
39
Q

Which are the main poor prognosis markers of chronic hepatitis?

A
  • Hyperbilirrubinemia
  • Hypoalbuminemia
  • Prolongation coagulation times
  • Ascites (except in cocker)
  • Extent of fibrosis
40
Q

Which are the main primary and secondary bile acids?

A
  • Primary: cholic acid and chenodeoxycholic acid
  • Secondary: deoxicholate, lithocholate
41
Q

Which is the most difference between Caroli syndrome and Caroli disease?

A

Caroli disease is the presence of large intrahepatic cysts.
Caroli syndrome is the presence of these cysts + congenital hepatic fibrosis + CKD.

42
Q

Which is the etiopatogeney of canine neutrophilic cholangitis?

A
  1. Functional/mechanical biliary tract obstruction –> decreased enterohepatic circulation of bile –> increase intraductal pressure –> reduction in antimicrobial properties –> bacterial translocation
  2. Bacteria proliferation in bile:
    —- Ascendent from duodenum (less common in dogs due to low bacterial charge in duodenum and high power Oddi sphincter)
    —- Hematogenous

In dogs there is a high frequency of concurrent gallbladder diseases (cholecystitis, mucocele, stones, neoplas…) <– predispose to neutrophilic cholangitis due to bile stasis and bacteria nidus.

43
Q

Which is the prevalence of healthy dogs with bactibilia?

A

10%

44
Q

Which are the most prevalent bacterias found in a dog with neutrophilic cholangitis?

A

E Coli, Clostridium, Enterococcus

45
Q

Which is the definition of a neutrophilic and destructive cholangitis?

A
  • Neutrophilic: neutrophilic inflammation in the bile ducts epithelia or lumen.
  • Destructive: destruction and loss of bile duct epithelia + inflammation and fibrosis
46
Q

Which are the suggested hypothesis of destructive cholangitis?

A

Idiopathic vs drug induced (sulfonamides, amoxiclav) vs infectious (Distemper)

47
Q

Which is the immunohistochemistry used to detect destructive cholangitis?

A

Cytokeratin 7 (biliary epithelial marker)

48
Q

Which are the most common hepatobiliary diseases in dogs?

A

Reactive hepatopathy > chronic hepatitis > acute hepatitis

49
Q

Which is the suggested etiopathogenesis for a intrahepatic colelithiasis in dogs?

A

There is a change in the composition of the bile due to cholestasis/mucus hypersecretion/infection/etc.
It use to go concurrently with cholelithiasis and gallbladder diseases because the mentioned predisposing factors also predisposed these diseases.

50
Q

Whihc is the mechanism of formation of secondary bile acids?

A

LIVER:
Cholesterol –> BA –> conjugated with glycine/taurine –> conjugated BA (primary BA: cholic acid and chenodeoxycolic acid) –> GB –> duodenum
DUODENUM:
Most of the primary GB secreted are reabsorbed in the ileum.
A small fraction of BA are deconjugated (unconjugated BA) or hydroxilated (secondary BA: deoxycholate and lithocholate) in the intestinum –> reabsobed

51
Q

Which are the beneficious effects of primary bile acids?

A
  • More hidrophilic –> promote the biliary excretion
  • Less toxic –> reduce inflammation
  • Increase fat absorption

–> if there is a taurine deficit and BAA cannot be conjugated –> increase deconjugated BA –>
- Less biliary excretion –> increase serum BA
- Increase inflammation
- Hypocholesterolemia due to reduce fat absorption

52
Q

Which is the main difference in the diagnosis of neutrophilic cholangitis between dogs and cats?

A

Increase hepatic enzymes is very specific in dogs, and the pattern is most commonly cholestatic.
In contrast, due to the lower half life in cats, its sensibility is lower (can be causes with hepatic enzymes on range) and there are not often convincingly cholestatic.

53
Q

Which are the most reliable markers of EHBDO in cats?

A
  • CBD dilation >5mm
  • Dilation of intrahepatic bile ducts
  • Presence of a obvious source of obstruction

Gallbladder dimensions doesn’t like to be a reliable indicator

54
Q

Which are the most common vitamins affected in a hepatobiliary disease?

A
  • Liposolubles vitamin due to cholestasis (vitamin K specially –> can be supplemented)
  • Hydrosolubles (because the liver is essential for storage and activation): vitamin B
    —- B1 (thiamine) –> can be supplemented
    —- B12 (cobalamin) –> can eb supplemented
55
Q

Which are the potential causes why corticosteroid at antiinflammatory doses can improve the course in a cat with neutrophilic cholangitis non responsive to ab?

A
  • Reduce inflammation of organs related to liver (pancreas, intestine)
  • Potential immunomediated rol in the etiology
  • Reduce edema
56
Q

Which is the main difference between lymphocytic and neutrophylic cholangitis?

A
  1. The histopathology
  2. The CBC (unremarkable in LC and inf/septic in NC)
57
Q

Which is the prednisone treatment regimen for a lymphocytic cholangitis?

A

If bile cultures are positive:
- Start at antiinflammatory doses together with 4-6w ab
- Once finished the ab, increase to immunosupressors doses

If bile cultures are negative:
- Start at immunosupressor doses, together with 2w of ab

4-6m

58
Q

Which is the reccommended treatment for feline fluke cholangitis?

A
  • Praziquantel: at t0 and 12w later (can continue to excrete eggs until 9w post tt)
  • Glucocorticoids at antiinflammatory doses
  • Antibiotics (because it can predispose to secondary infections)
  • Support tt
59
Q

Which are the methods to reach a definitive diagnosis in the fluke cholangitis?

A
  • Bile cytology: detection of eggs (S~100%)
  • Fecal analysis: detection of eggs (but low S~35%)
60
Q

Which is the distribution of tumors between dogs and cats?

A

Dogs:
- Methastatic (spleen, GI, pancreas) > primary
- Hepatocellular
- Malignant > benign

Cats:
- Primary > methastatic
- Billiary
- Benign > Malign (but in doubt)

61
Q

Which lineages of HCC can be distinguished in the dog?

A
  • < 5% kit19 positivity:
    —- Derived from mature hepatocytes
    —- More differentiated
    —- Less methastases
  • > 5% kit19 positivity:
    —- Derived from hepatic precursor cells
    —- Less differentiated
    —- More methastases
62
Q

What is a triaditis and which is the ethiology?

A

It is the concurrent inflammation of biliary tract, pancreas and intestine.
The exact ethiology is not known, but it is suggested to be secondary to a infectious/immunemediated/physical process. Due to the biliary anatomy of the cat, there is a high possibility of communication between the different organs.

63
Q

Which breeds are predisposed to mucocele?

A

Sheetland, Cocker, Miniature Shnauzer, Pomerania…

64
Q

Which is the etiology of mucocele?

A

Change in gallbladder secretory pattern:
- Hypersecretory phenotype
- Gel-like mucin

Due to:
- Increase hydophobic bile acids (toxics –> irritation gallbladder wall –> hypersecretion mucin + reduce smooth muscle contraction)
- Gallbladder hypomotility –> bile accumulation

Causes:
- Hypercholesterolemia and hypertrygliceridemia
- Hypothyroidism/Cushing/DM
- Increase leptin levels
- Reduced vitamin D

65
Q

Which are the different types of mucocele?

A
  • Type I: gravity independent sediment occupying more than 30% of gallbladder lumen
  • Type II: partial stellate
  • Type III: stellate
  • Type IV: combination of stellate and kiwi
  • Type V: partial kiwi
  • Type VI: complete kiwi
66
Q

How is the hemostatic pattern in cholestatic diseases in cats?

A

Can be both hypo or hypercoagulable, and tends to be hyperfibrinolytic

67
Q

Which is the probability that a clinical gallbladder mucocele rupture in the future?

A

50%

68
Q

Why a gallbladder mucocele perforation predispose to septic peritonitis?

A
  1. Due to rupture of a septic mucocele (cholecystitis)
  2. Due to liberation of bile acids (toxic/irritant –> increase permeability –> bacteria translocation)(bile acids impaired immune system)
69
Q

Which is the prevalence of positive gallbladder culture from cholecystectomy?

A

15%

70
Q

Which are negative prognostic indicators for survical in dogs with GBM that have a cholecystectomy performed?

A
  • Gallbladder rupture
  • Presence of clinical signs
  • Increase ALP and hyperbilirrubinemia
  • Increase lactate and hypotension
  • Pomerania
  • Higher age
  • Higher GMB grade
  • Concurrent hyperadrenocorticism
71
Q

Which is the association between celiachysm and GBM?

A

Border Terriers with GBM have higher levels of transglutaminase (+/- glyadin) and low levels of CCK –> GB hypomotility

72
Q

Which electrolytic disorder is associated with an increased risk of death postcholecystectomy?

A

HyperNa

73
Q

How is the distribution of biliary neoplasms in dogs?

A

Intrahepatic > Extrahepatic (GB > CBD)

  • Intraheptic the most common is colangiocarcinoma > carcinoid
  • In GB the most common is carcinoid
  • In CBD the most common is the carcinoma
74
Q

Which are the components of bile?

A
  • Cholesterol
  • Bile salts
  • Lecithin
  • Phospholipids
75
Q
A

Certifying Examination (10 decks)

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