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Smith LA Medicine > Ch 33 Hepatobililary > Flashcards

Ch 33 Hepatobililary Flashcards

1
Q

Where does most cell regeneration occur in the liver?

A

Rappaport’s zone 1 (portal). Then cells are pushed to the central lobular area.

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2
Q

At what point post product administration does acute serum hepatitis occur?

A

4-8 weeks

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3
Q

Which clotting factors are produced by the liver?

A

Factors I, II, V, VII, IX, and X

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4
Q

Briefly, what is the pathogenesis and common differential diagnoses for equine icterus?

A

Failure of uptake, conjugation, or excretion of bilirubin.
Massive hemolysis, bile blockage, equine fasting/anorexia

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5
Q

Briefly, what is the pathogenesis and common differential diagnoses for bovine ascites?

A

Portal hypertension and lymph leakage via cirrhosis or veno-occlusion.
Cardiac failure, hypoproteinemia, cushing’s syndrome

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6
Q

How do you diagnose hepatic encephalopathy?

A
  1. Blood ammonia: liver isn’t metabolizing it to urea. But poor correlation
  2. Clinical signs: neurologic, ruminants show tenesmus or vocalize. Horses develop central blindness or headpress, excitable
  3. Possibly postmortem: increased CSF glutamine?
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7
Q

Which are the hepatic ‘leakage enzymes’? What do they indicate, respectively?

A

AST, SDH, GLDH, LDH. Indicate hepatocellular injury or necrosis
1. Aspartate aminotransferase: From liver, muscle, erythrocytes, and heart.
2. Sorbitol dehydrogenase: Short t-1/2, acute dz indicator. Liver-specific. May elevate due to dehydration or hypoxia, not liver disease necessarily

  1. Glutamate dehydrogenase: Liver-specific, not elevated in chronic dz
  2. Lactate dehydrogenase: Not specific. Short 1-1/2. Also in erytrocytes
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8
Q

What are the ‘cholestatic’ enzymes? What do they indicate?

A

GGT (gamma glutamyltransferase): Liver-specific. High in colostrum-drinking neonates. May elevate with colonic displacement due to bile duct compression.

ALP (Alkaline phosphatase): Liver, bone, intestine, macrophages, placenta. Nonspecific.

Both more likely to elevate in chronic disease. Associated with biliary obstruction

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9
Q

What is the most sensitive indicator of liver disease in the horse?

A

GGT. Levels stay elevated for weeks

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10
Q

What can serum urea nitrogen indicate in liver disease. How can it be misleading in cattle?

A

SUN/BUN: Liver produces urea, so if SUN drops, could indicate liver disease. HOWEVER, can also drop if a ruminant is off feed, because the bacteria are using it all to make protein

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11
Q

What is the half life of albumin in the horse vs cattle and sheep?

A

Horse: 19.4 d
Cow: 16.5 d
Sheep: 14 d

Reduced in chronic liver disease

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12
Q

What type of amino acid increases in liver disease?

A

Aromatics… short branched chain aa’s are decreased

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13
Q

How can bilirubin indicate liver damage? What does it tell you?

A

-Incr bilirubin ddx: liver failure, bile blockage, hemolysis, or fasting (horse).

-In horse/cattle, rising bilirubin = retained unconjugated BIL. The direct(conjugated) to Tbil ratio can also rise in liver disease.
-Bile blockage/intrahepatic cholestasis increases Direct: total ratio
-Increased DIRECT(conjugated) bil usually due to hemolysis
-Blocked bile ducts will increase the conjugated AND unconjugated bil
-Equine TBil increases with fasting due to reduced removal.
-Normal ruminant Tbil is low
-

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14
Q

Which is the most sensitive indicator for liver function?

A

Bile acids. In horses, > 20 umol/L is specific for nonsurvival.
Cattle have much higher ranges

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15
Q

What indicators would spell a poor prognosis in liver disease?

A

-Albumin < 2.5 or incr. globulin
-Prothrombin time > 30% normal
-Greatly elevated GGT, ALP, with normal or decreased SDH or LDH.
-Marked fibrosis
-Signs of hepatic encephalopathy

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16
Q

Where are liver biopsies collected in the horse?

A

Horse: R 14th IC space, at intersection of tuber coxae to point of shoulder. Needle directed slightly cranial-ventral, with US guidance

Cow: 11th right ICS intersected with horizontal line from PL fossa

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17
Q

How is idiopathic acute hepatitis/Theiler’s disease, diagnosed in horses?

A

Bloods: high UC or total bilirubin, high bile acids and hepatocellular & cholestatic enzymes. Low BUN, hyperammonemia, prolonged clotting time, decr albumin

PCR for serum or liver Equine parvovirus-hepatits

Biopsy: Centrilobular & midzonal necrosis. Pale, eosinophilic granular mass outlining necrotic hepatocytes.

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18
Q

What causes infectious necrotic hepatitis/black disease? How does it cause disease?

A

-Clostridium novyi type B. Exotoxins alpha and beta
-Occurs when larval migration of liver flukes has created damage enough for an anaerobic environment
-Patho: Alpha toxin and beta toxin:
Alpha toxin inhibits guanosine triphosphatases by glycosylation
Beta toxin is a necrotizing lecithinase.

Enters animal by ingestion from soil, then disseminates into kupffer cells and whole macrophage system. Anaerobic conditions allow spores to vegetate and proliferate, release toxins –> coagulative necrosis, then exotoxins disseminate. Sudden death

19
Q

How is Black disease diagnosed?

A

Necropsy: areas of coagulative necrosis yellow-white, with hyperemic zones
+
Isolating C. novyi type B from the liver: culture, fluorescent antibody ID of impression smears, toxin ID
OR: gram stain an impression smear to find gram positive rods,

20
Q

What is the pathogenesis of bacillary hemoglobinuria?

A

Agent: Clostridium haemolyticum. Has a beta toxin, a phospholipase C causing hepatocyte necrosis, hemolysis, and damages capillary endothelium. Causes hepatic necrosis and intravascular hemolysis.
-Sudden death in cattle and livestock
-Assoc with fluke migration
-Ingested from soil, hangs out in macrophages, lives in kupfer cells for long time. Localized anaerobic liver area leads to spore germination, proliferation, toxin production, necrosis, and thrombus formation

Animals > 1 yr old.

21
Q

How do you diagnose bacillary hemoglobinuria?

A

Bloods: Incr hepatic enzymes and TBil. PCR for organism and toxin (cattle).
Urine: Hemoglobinuria.
Smears: blood, peritoneal fluid, liver, or spleen.
Necropsy: Fluorescent antibody tests on impression smears from a liver ‘infarct’.

22
Q

How should liver enzymes and indicators be interpreted in the neonatal foal?

A

-TBil is incr due to converting fetal hemoglobin to adult
-ALP incr due to osteoblasts
-GGT elevated for 2-4 weeks (but only slight in SDH).
-Serum bile acids incr for first 6 weeks

23
Q

What is Tyzzer’s disease, and what is its pathophysiology?

A

-Acute hepatitis of foals 7-42 d old
-Blame: Clostridium piliforme. Gram neg, flagellated, intracellular obligate anaerobe
-Isolates E and R1 usually in horses
-Die in 2-48 hours. Spontaneous or in outbreaks.
-Contributors (patho unknown): young dams, high protein diet to dams, crowded conditions,

24
Q

How would you diagnose Tyzzer’s?

A

-Cx: neuro, colic, found dead, fever.
-Overwhelming sepsis
-Incr bile acids, bili, liver enzymes,

*Necropsy: Acute, widespread multifocal necrosis and hepatitis. Filamentous bacteria at lesion periphery. Silver or giemsa stain.

25
Q

How might late-term infection with EHV-1 affect a weak but live-born foal?

A

-Severe, multifocal necrotizing hepatitis with inclusion bodies.
-NOT elevated liver enzymes
-General respiratory distress

26
Q

How are neonatal isoerythrolysis and liver failure related? What causes this and how can you reduce the risk?

A

-Multiple blood transfusions (esp if 4L+) can cause iron overload, and chronic hypoxia from NI can cause liver failure

-Deferoxamine: iron chelator increases urinary iron clearance and prevents iron tox in healthy foals. Give 12hr prior to transfusion

27
Q

What is kernicterus? How does it develop?

A

Bilirubin encephalopathy. Can result from NI as well because unconjugated bilirubin is toxic to the CNS.
-Esp if TBil > 27.

28
Q

How does iron toxicity occur in foals?

A

*Foals given iron before receiving colostrum!
See Cx 2-5 d later: hepatic encephalopathy, icterus, elevated GGT, ALP, ammonia, TBil, PCV. Seizures, depression, ataxia.
Small livers with prominent bile duct proliferation, hepatic cell necrosis, and changes in the brain

29
Q

What is the pathophysiology of pyrrolizidine alkaloid toxicity?

A

-Indirectly toxic; bioactivated via hepatic metabolism
-Pyrroles crossling double-strand DNA, then an antimitotic effect.
-Hepatocytes cannot divide so become megalocytes. When they die, they’re replaced by fibrosis
-Toxic effects seen when hepatonecrosis and fibrosis lead to loss of function

Downstream effects: Fibrosis disrupts bloodflow, prevents regeneration and leads to portal hypertension.
-Ruminants: see diarrhea and ascites, rectal prolapse, weight loss, tenesmus
-Horses: neuro signs, weight loss, slight icterus.

30
Q

What are the clinical signs of fasciolosis in ruminants? What aspects of fluke infestation cause these?

A

Proliferative cholangiohepatitis
Cattle
1. Nutritional stress: less fertile, longer calving interval, lightweight calves
2. Anemia: blood feeding flukes
3. Depression, anorexia, anemia, biliary hyperplasia: Proline, from fluke metabolism

Sheep/goats: most damaged
-Fatal ascites, abdominal hemorrhage, pallor, icterus: massive fluke entry into bile ducts 6-10 weeks post infection
-Chronic: submandibular edema, ascites, emaciation

31
Q

How do you diagnose fluke infestation?

A

Fecal sedimentation
High probability of losses indicated when >10 eggs per 2gram.
*also elevated GGT, GDH, eosinophilia
Eggs are amber, larger, and more rounded at the operculum than Paramphistomum eggs

31
Q

How do you diagnose PA toxicity?

A

Vague: Elev GGT and ALP. Bile acids&raquo_space;>
Inc bilirubin later.
*Biopsy or necropsy shows:
1. Fibrosis
2. Bile duct proliferation
3. Megalocytosis

32
Q

Which organism is most commonly implicated in bovine hepatic abscesses, and what are the virulence factors?

A

Fusobacterium necrophorum: gram neg, pleomorphically rod-shaped anaerobe.
(also in calph diphtheria, footrot)

Normally inhabits the rumen, in higher conc in cattle fed more grain (starch).

Virulence factors: MANY. But Leukotoxin is #1.
Subspecies necrophorum produces more leukotoxin.
Subspecies funduliforme produces less.

Enters portal blood through damaged rumen (rumenitis), establishes infection in the liver.

**THere’s a vaccine targeting leukotoxin and outer membrane proteins!

33
Q

Which is the second most commonly isolated organism in bovine hepatic abscesses?

A

Trueperella pyogenes: gram pos rod.
-Esp likes the ruminal wall
-Facultative aerobe

34
Q

What, in brief, is the pathophysiology of bovine hepatic abscesses? How do bacterial virulence factors play a role in this?

A
  1. Sudden change to high energy diet or other cause of rumenal acidosis or ingestion of damaging materials.
  2. Damaged rumen wall is susceptible to colonization by F. necrophorum
  3. F. necrophorum accesses blood, makes rumenal wall abscesses, and sheds bacterial emboli to portal circulation
  4. Bacteria filtered by liver

NOW THE VIRULENCE FACTORS
1. proteases, dermonecrotic agents, cytotoxic allows further rumen wall damage
2. Leukotoxin prevents phagocytosis
3. Release cytolytic products that damage liver
4. Makes itself an anaerobic environment by killing other cells

35
Q

What are the most commonly isolated bacteria in equine hepatic abscesses?

A

Strep equi, E coli, bacteriodes fragilis, etc

36
Q

What are the primary prepartum risk factors of hepatic lipidosis?

A

BCS > 4.0; severe feed restriction, excess feed energy, long calving intervals

37
Q

What are the postpartum risk factors of hepatic lipidosis?

A

Concurrent diseases, reduced DMI, sudden changes in feed

38
Q

What are the risk factors in does and ewes for pregnancy toxemia?

A

Ewes: 2 or more lambs
Dose: 3 or more kids
Both: last 2-4 weeks gestation, obese dam, poor quality feed, cold weather, lack of exercise, stress of movement during risk period, excessively thin does/ewes

39
Q

How do you diagnose pregnancy toxemia?

A

Ketones in urine before detected in blood.
-Acidosis, low Calcium and potassium
BHB > 1 mmol/L

40
Q

What are the primary causes of equine hyperlipidemia?

A

Overproduction of VLDL, especially the abnormal type VLDL1 with reduced apolipoprotein B100 and B48 content, which enables greater TG content

Decreased caloric intake.

41
Q

How do you diagnose hyperlipemia?

A

Triglycerides in serum > 500
Opaque/fatty plasma , fatty liver and kidneys on necropsy

42
Q

What triad of clinical signs indicates equine cholelithiasis?

A
  1. Recurrent colic
  2. Intermittent pyrexia
  3. Icterus
43
Q

Where are choleliths more likely to be seen on ultrasound?

A

The cranioventral right hepatic lobe, ICS 6-8
Also see dilated bile ducts

Smith LA Medicine (12 decks)

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