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Canine/Feline Internal Medicine > Liver/Pancreas > Flashcards

Liver/Pancreas Flashcards

1
Q

Explain consequences of portal hypertension secondary to liver disease.

A

From obstruction/reduced blood flow through the liver.
Can cause ascites (abdominal effusion).
Sequale to chronic liver disease (because so cirrhotic)

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2
Q

How can liver disease result in abdominal effusion?

A

Usually transudate fluid from pressure change, hypoalbuminaemia, vascular permeability change.

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3
Q

What causes icterus? Be specific.

A

Excessive haemolysis
Choleostasis
Liver damage

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4
Q

What causes hepatomegaly and how would you recognise this?

A 
Hepatic lipidosis 
Hepatotoxicity 
Neoplasia
Passive congestion 
Amyloidosis 
Recognise by palpation, radiography, ultrasound, CBC, biochem, FNA, cytology.
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5
Q

What is your diagnostic approach to an icteric cat/dog.

A 
Do PCV and blood smear (anaemia) 
CBC, biochem, urinalysis (hepatocellular  cholestatic enzymes, liver functon) 
Imaging
FNA
Ex lap
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6
Q

What is hepatic encephalopathy? What diseases result in this? What pathophysiological mechanisms?

A

HE is abnormal neuro signs secondary to hepatic dysfunction.
Caused by reduction in functional liver mass or portal blood bypasses the liver.
Liver fails to convert ammonia, increase amino acids…
Can get ammonium biurate crystals in urine (no ammonia conversion)

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7
Q

What mechanisms contribute to GI bleeding in patients with liver disease?

A

Coagulation factors 2, 7, 9 & 10 are synthesised in the liver vitamin K dependent.
Portal hypertension can cause vascular congestion, biliary obstruction, poor mucousal perfusion.

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8
Q

What occurs if portal blood bypasses the liver?

A

Hypoperfusion of the liver means that circulation cannot be detoxified.

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9
Q

Which breeds are predisposed to copper storage disease/accumulation?

A

Bedlington Terrier, Sky terrier, Dalmatian, Siamese cats

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10
Q

What are the liver enzymes we test for and what do they indicate?

A

ALT (liver), AST (muscle), ALP (cholestasis, bone), GGT (choleostasis, biliary, renal tubules, mammary).
These indicate hepatocellular/biliary damage. NOT liver function.

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11
Q

What are some indicators of hepatic synthesis & homeostasis and why?

A

Urea - liver converts to ammonia normally
Albumin/Globulin - No albumin synthesis
Glucose - severe hepatic loss failure glucose homeostasis
Cholestrol - hypo or hyper depending
Coagulation factors - 2, 7, 9 & 10.
Potassium - most common electrolyte disorder

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12
Q

What is the normal bilirubin content in urine for dogs?

A

1+ or 2+

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13
Q

Why do we test serum bile acids?

A

Test for clinically significant hepatobiliary disease/ portosystemic shunting.
Bile acids synthesised in liver secreted in bile. Don’t measure if choleostasis is present.

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14
Q

What is the most common liver disease in dog?

A

Chronic parenchymal disease

Leads to fibrosis & cirrhosis

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15
Q

What is the most common liver disease in cats?

A

Primary biliary disease

And hepatic lipidosis

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16
Q

What characterises chronic hepatitis?

A

Necrosis
Inflammation
Regeneration & fibrosis
Then get portal hypertension (ascites, HE), pain, pyrexia, gastric ulceration)

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17
Q

How do you diagnose chronic hepatitis?

A

ALT elevated initially (then will get lower as more liver destruction)
Low urea & albumin
Coagulation
Biopsy

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18
Q

How would you treat chronic hepatitis?

A

Diet high quality protein + veges
Antioxidants
Glucocorticoids (anti-inflammatory, anti-fibrotic)
Antibiotics NOT hepatotoxic

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19
Q

What’s the difference between true and secondary copper storage disease?

A

True - dogs can’t process copper eg. Bedlington Terriers

Secondary - chronic hepatitis causes copper accumulation eg. Dalmatian

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20
Q

How do you manage Cu storage disease/accumulation?

A

Low Cu high Zn diet
Bottled water
Copper chleation `

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21
Q

Compare acute and chronic hepatitis.

A

Acute - uncommon, infection/toxin insult (adenovirus or aflatoxins), fast & severe loss function, severe icterus
Chronic - common, idiopathic, slow, regeneration & fibrosis, ascites, pain, pyrexia, no icterus.

22
Q

What’s the prognosis for acute hepatitis?

A

Okay due to regeneration capability.

Put intensive supportive care.

23
Q

Describe a congenital portosystemic shunt. What do you look for and how would you treat it?

A

Blood bypasses the liver. Most common congenital form.
Get no ascites, small runty dogs with poor growth, PU/PD, no enzyme elevation (liver not damaged).
Treat with gradual occlussion and surgical ligation so other vessels can open back up slowly eg. ameroid constrictor.

24
Q

What condition ultrasonographically looks like a slice of kiwifruit with striations?

A

Gall bladder mucocoele.

Result of inflamation or motility disorder.

25
Q

What are some reasons for a nodular appearing kidney?

A

Cirrhosis, regeneration, hyperplasia, neoplasia.

26
Q

How does hepatic lipidosis occur?

A

From obesity - excess fat is mobilised to the liver.

Or associated with anorexic cat.

27
Q

Middle age cat recently moved house has intermittent vomiting, dehydration, diarrhoea and constipation. What are you thinking?

A

Recent stressful event.
Could be hepatic lipidosis. Check if icteic, coagulopathy, hepatomegaly.
Diagnose with ALT, AST, ALP are elevated, radiograph.
Treat with intensive high protein feeding, oesophagostomy tube might be option, don’t force feed cats, cobalamin.

28
Q

What common feline disease is associated with triaditis and why?

A

Biliary tract disease because biliary and pancreatic ducts join before entering duodenum.

29
Q

How do you differentiate neutrophilic and lymphocytic cholagnitis?

A

Histopathology. Must take really good samples via exploratory laparotomy.
Neutrophilic is suppurative, lymphocytic is not.

30
Q

How do you treat neutrophilic cholangitis?

A

Neutrophilic infiltration bile ducts!
IV fluids, antibiotics based on samples, nutritional support & ursodeoxycholic acid (ursofalk - bile acid reduces bile toxicity & waters down bile).

31
Q

What is your main DDx for lymphocytic cholangitis?

A

Hepatic lymphoma

32
Q

What is the prognosis if the liver survives an acute insult?

A

Good prognosis - regeneration can occur.

33
Q

Why must care be taken when giving fluids to ascites patient?

A

Hypoproteinaemia - easy to flood animal full of fluids

34
Q

What is your fluid choice for most liver conditions?

A

Fluids with potassium supplementation.
NOT lactated ringers.
Saline or Hartmans.

35
Q

What is your main antibiotic of choice for liver conditions?

A

Broad spectrum use Amoxycillin/Clavulanate or Metronidazole

36
Q

What’s your approach to nutrition of liver disease?

A 
High quality protein (no excess NH4)
Good calories (metabolism) 
Fluids
Antiemetics
3-8 small feeds through day
37
Q

How do you manage portal hypertension & ascites?

A

Vitamin K
Good quality protein feeding
Frusemide, spirolactone
Potassium therapy

38
Q

Describe the pathogenesis of exocrine pancreatic insufficiency.

A

Lack of pancreatic enzymes resulting in maldigestion.
Get weight loss, greasy fatty stools, no absorption of food.
Caused by pancreatic acinar atrophy (immune mediated) or chronic pancreatitis.

39
Q

Why is cobalamin required?

A

For vitamin B12 absorption. Made in the pancreas.

40
Q

Animal has weight loss with good nutrition. What do you suspect?

A

EPI (maldigestion)
Small intestine disease (malabsorption)
Metabolic (malutilisation)

41
Q

How do you rule of EPI when diagnosing an issue?

A

Serum trypsin-like immunoreactivity.

Produced by pancreas into serum

42
Q

What is your choice of EPI treatment?

A

Pancreatic enzyme supplementation
Metronidazole antibiotic for any bacterial overgrowth small intestine (SIBO)
Cobalamin
Diet management (not too much fat, low fibre)

43
Q

Why is chronic pancreatitis uncommon?

A

Hard to diagnosis very non-specific waxing/waning with mild clinical signs.
Diagnose only really by biopsy or laparotomy.
Test canine pancreatic lipase immunoreactivity - specific circulating enzyme

44
Q

What is the aetiopathogenesis of acute pancreatitis?

A

Premature trypsin activation causing autodigestion and inflammation. Protective mechanisms get overwhelmed and get inflammation & pancreatic failure.
90% idiopathic

45
Q

What is your main DDx of acute pancreatitis?

A

Upper GI obstruction.

46
Q

What is the best way to test for acute pancreatitis? And chronic pancreatitis?

A

Canine pancreatic lipase immunoreactivity or feline.

Sensitivity reduced in mild or chronic forms.

47
Q

What are the mainstays of treating acute pancreatitis?

A

IV fluids, analgesia & early enteral feeding

48
Q

Why is diagnosis of pancreatitis harder in cats than dogs?

A

Less obvious clinical signs even when very severe cases. Can also be complicated by triaditis.

49
Q

What is triaditis? What is aetiopathogenesis and how would you diagnose and treat it?

A

Combination of biliary disease, IBD & pancreatitis in cats.
Neutrophilic or lymphocytic main types.
Do biopsy of pancreas. High ALT, neutrophilia, cytology.

50
Q 
Define the following: 
Ammonium biurate crystals 
Bilirubin cystals
Ursodeoxycholic acid
S-adenosyl methionine
Silymarin 
Lactulose
cPLI test
Pancreatic enzyme supplement
A

Ammonium biurate crystals - produced from hyperammonia esp portosystemic shunt
Bilirubin cystals- hyperbilirubinaemia cases
Ursodeoxycholic acid- bile acid makes bile watery and less toxic.
S-adenosyl methionine- metabolic for hepatic function
Silymarin - Milk thistle antioxidant
Lactulose- non absorbable sugar for consiptation
cPLI test- canine pancreatic lipase immunoreactivity test for pancreatitis
Pancreatic enzyme supplement - give to EPI patients

Canine/Feline Internal Medicine (9 decks)

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