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Alimentary > Icterus/HE in small animals > Flashcards

Icterus/HE in small animals Flashcards

1
Q

In what form in newly formed unconjugated bilirubin?

A

insoluble in water, bound to albumin, dissociates from this before entering liver cell

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2
Q

What happens to bilirubin in the liver cell?

A

Conjugation with glucoronic acid making it water-soluble for excretion in urine (rate limiting step in hepatocyte)

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3
Q

What do bacteria in the lower urinary tract do?

A

convert bilirubin into urobilinogen –> enterohepatic circulation

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4
Q

Define pre-hepatic icterus

A

conjugation and uptake of bilirubin into liver overwhelmed

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5
Q

Define hepatic icterus

A

uptake, conjugation and excretion of bilirubin in hepatocytes overwhelmed

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6
Q

Define post-hepatic icterus

A

conjugation, excretion and uptake back into liver overwhelmed

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7
Q

What signs might show clinical signs of icterus? 4

A
  • GIT
  • neurologic
  • renal/urinary
  • haematologic
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8
Q

GIT signs 4

A
  • vomiting and diarrhoea (common)
  • acholic faeces (i.e. white)
  • melaena
  • ascites
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9
Q

Neuo signs of HE 6

A
  • personality change
  • ptyalism (drooling, cats)
  • head pressing
  • disorientation
  • seizures
  • stupor
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10
Q

Renal signs 6

A 
Pu/PD (insufficient urea to concentrate)
pollakiuria
stranguria
dysuria
bilirubinuria
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11
Q

Define pollakiuria

A

excessively high daytime frequency of urination

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12
Q

Define stranguria

A

slow, painful urination caused by mm spasms of the urethra and bladder

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13
Q

Define dysuria

A

painful micturition

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14
Q

Haematologic signs 6

A
  • yellow animal
  • pale MM
  • anaemia from GIT haemorrhage
  • anaemia of chronic disease
  • coagulation disorder
  • haemolysis
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15
Q

DDx for pre-hepatic icterus

A

Haemolysis (IMHA, babesia infection, toxins - onions, lead , copper)

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16
Q

DDx for hepatic icterus - CAT 6 (in order of likelihood)

A
  • suppurative cholangiohepatitis
  • lymphoplasmacytic hepatitis
  • hepatic lipidosis
  • FIP
  • toxins (acetaminophen=paracetamol, aspirin)
  • neoplasia
17
Q

DDx for hepatic icterus - DOG 4 (in order of likelihood)

A
  • acute liver disease
  • leptospirosis
  • chronic hepatitis
  • neoplasia
18
Q

DDx for post-hepatic icterus (both dogs and cats) 3

A
  • pancreatitis
  • neoplasia (liver, duodenum, pancreas - i.e. close anatomic proximity)
  • cholelithiasis (uncommon in cats/dogs)
19
Q

How do you differentiate pre-hepatic and hepatic icterus? 2

A

PCV and TS (Prehepatic: PCV is low, TS normal. Hepatic - PCV usually normal, TS can be low if albumin is low)

20
Q

How do you differentiate hepatic and post-hepatic icterus?

A

Imaging (what the bile duct looks like, what’s blocking it perhaps, pancreatitis etc.)

21
Q

Describe the workup for hepatic diseases - 8

A
  • haematology, chemistry profile, UA
  • liver function tests
  • coagulation tests
  • abdominal ultrasound
  • aspirate effusion, cytology
  • liver fine needle aspirate
  • fine needle aspirate and culture of bile
  • liver biopsy (histology, culture)
22
Q

What is the most specific liver enzyme?

A

ALT (increased means increased numbers of hepatocytes are dying)

23
Q

Where is AST present?

A

Liver but also the mm and intestines

24
Q

What is AP and where is it found?

A

Alkaline phosphatase. Found in biliary duct cells (which are throughout the liver). Isoenzymes of this are cortisol-induced (dogs only) in bone, intestines, liver, placenta etc

25
Q

Indications for liver failure on biochemistry - 4

A

-Low albumin
-Low cholesterol
-low glucose
-low BUN
(be sure to run a bile acid test as well)

26
Q

Where are bile acids produced? From what?

A

in liver from cholesterol

27
Q

How do bile acids return to the liver after secretion into small intestine?

A

enterohepatic circulation

28
Q

How do you measure bile acids? When do levels of this change?

A

Take two measurements:
1st = fasted
Give food then take 2nd measurement
The rate limiting step ins the re-uptake of bile acids from the blood into hepatocytes. Levels are elevated in liver failure and PSS.

29
Q

What is HE

A

ammonia and aromatic AA go directly into blood without passing through liver first means the CNS is exposed to shunted gut-derived toxins

30
Q

Neurologic signs of HE - 5

A
  • bizarre behaviour
  • head pressing
  • seizures
  • intermittent blindness
  • ptyalism (cats)
31
Q

Signs of urate stone formation 3

A

dysuria, stranguria and haematuria

32
Q

Clinical sign of HE

A

urate stone formation

33
Q

Pathogenesis of urate stone formation

A

increased ammonium concentration in blood, decreased ability to convert uric acid to allantoin in the liver –> more urate excreted in urine

34
Q

Most important diseases causing HE in CATS - 4

A

acute liver failure (toxic)
hepatic lipidosis
neoplasia
PSS (v rare in cats)

35
Q

Most important diseases causing HE in DOGS - 3

A 
PSS
liver failure (acute) - toxic, infectious
liver failure (chronic) - cirrhosis
36
Q

In hepatic acidosis, how can FFA and Tg be processed by liver? When doesn’t this work? Treatment?

A
  • B oxidation
  • redistribution to other organs via lipoproteins (especially VLDLs)
  • doesn’t work if diet is protein-deficient. Treatment therefore requires force-feeding (stomach tube) diet which is high in protein.
37
Q

How do you test for liver function?

A

bile acids (remember 2 readings). Not liver enzymes as these won’t tell you if the whole liver is working.

38
Q

What are classic biochemistry signs for HE? 3

A

low glucose and urea, high bile acids (latter confirms hepatic dysfunction)

39
Q

DDx for seizures/strong reaction to normal diazepam dose, decreased mentation, lethargy, weakness, inappetence?

A

INTRACRANIAL:

  • anomaly (hydrocephalus, lissencephaly)
  • infection (distemper, toxoplasma, parasites)
  • idiopathic epilepsy
  • trauma

METABOLIC:

  • EXOGENOUS - toxic - medications
  • ENDOGENOUS - HE because PSS, uraemia, electrolyte disturbances, hypoglycaemia

Alimentary (37 decks)

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