Hepatic And Pancreatic Disorders Flashcards

1
Q

What would happen if blood flow through the liver was obstructed

A

Portal venous hypertension and translation of fluid

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2
Q

What if portal blood bypassed the liver?

A

Hypoperfusion of the blood through the liver and the blood would not be detoxified
Portosystemic shunt

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3
Q

How might hyper bilirubinaemia occur

A

Haemorrhage or haemolysis
Excessive RBC breakdown
Hepatocytes can’t break it down
Bile duct blockage

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4
Q

What would be the systemic consequences of liver failure

A

Altered synthesis, conjugation, metabolism, gluconeogenesis, haematopoesis and storage

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5
Q

What are the two mechanisms in which liver disease may cause an enlarged abdomen?

A

Hepatomegaly

Involvement of liver in systemic disease causing a transudate

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6
Q

How might you be able to identify hepatomegaly?

A

Palpation- beyond the costal arches

Radiography- caudal displacement of gastric axis

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7
Q

In which species is abdominal effusion more common?

A

More common in dogs than cats

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8
Q

What are the different types of abdominal effusions and list a mechanism and characteristic for each

A

Transudate- caused by pressure differential and is clear to straw in colour with relatively low protein (common)
Non-septic exudate- inflam not caused by pyogenic infection with mod-high protein (FIP)
Septic exudate-inflame due to pyogenic infection with high to very high protein
Haemorhhagic- bleeding with predominately RBCs
Chylous- ruptured lymphatics with milky to creamy pink with high triglycerides
NB: protein under 30g/L is normal

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9
Q

Transudates are the most common abdominal effusion. What are the 5 mechanisms that can cause a transudate?

A

Increased Portal venous hydrostatic pressure- congestion or resistance in portal flow
Decreased intravascular oncotic pressure
Altered vascular permeability- perivascular inflammation
Insufficient resorption
RAAS activation- pooling of blood in splanchnic circulation causing hypotension

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10
Q

Define icterus/jaundice and what are the parameters that dictate where you will see it

A

Yellow staining of serum and or tissues by excess amounts of bilirubinaemia
0-10umol/L normal
25-50umol/L- yellow serum
50umol/L + -jaundice

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11
Q

How does bilirubin get into the blood stream

A

Breakdown of RBCs > haemoglobin > heme + globin
Globin > taken away by transferrin
Heme > biliverdin > unconjugated (free) bilirubin

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12
Q

What are the three major mechanisms by which hyperbilirubinaemia occur

A

Prehepatic- intra or extravascular haemolysis or haematoma, haemolytic anaemia and parasites
Hepatic- liver can’t process and secrete bilirubin, FIP
Post hepatic- biliary obstruction, cholangitis

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13
Q

When is bilirubinuria pathogenic in the dog and the cat

A

Dogs can have a normal dipstick finding of 2+

Always pathological in cats

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14
Q

What is the key diagnostic question in response to an animal with icterus

A

Is the cause prehepatic, hepatic or posthepatic

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15
Q

What test is able to rule out pre-hepatic causes

A

PCV/TP and blood smear to see if there is a regenerative anaemia

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16
Q

Would CBC, biochemistry and urinalysis be warranted in an icteric animal and why

A

Yes, assess liver function, inflammation and involvement of other organs

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17
Q

What diagnostic imaging technique would be most helpful and why

A

Ultrasound, assess many organ systems and may be able to differentiate between hepatic and post hepatic causes
Consider Ex lap and biopsy also for cats

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18
Q

What is hepatic encephalopathy and what is it caused by

A

HE is abnormal mentation and neurological dysfunction secondary to hepatic dysfunction
Due to the effects of endogenous toxins that the liver has not removed from circulation from decreased functional mass or portal blood bypassing the liver
Failure to convert ammonia to urea

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19
Q

What are some of the clinical signs of HE

A

Motor dysfunction- ataxia
Mentation- aggression
Seizures
Hypersalivation in cats

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20
Q

Which diseases are likely to cause HE

A

Acquired vascular shunting due to portal hypertension

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21
Q

How does liver disease cause GI bleeding

A

Liver is unable to produce clotting factors
Biliary rupture or obstruction prevents bile acids from breaking down fat, including vitamin K
Poor GI mucosal perfusion leading to ulcers

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22
Q

Are liver enzymes indicators of hepatocellular and biliary damage

A

Yes, but this gives no information on liver function or prognosis
Damage does NOT = function

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23
Q

Alanine aminotransferase (ALT)

A

Leaks from injured hepatocytes
Specific in dog and cat but can increase with muscle damage
Not useful in chronic conditions
Slight rise with some drugs- corticosteroids

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24
Q

Alkaline phosphatase (ALP)

A

Released due to cholestasis- sensitive indicator
Can indicate corticosteroid use or bone tumours
Can also indicate hepatic lipidosis or hyperthyroidism in cats

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25
Q

Gamma gluteryl transferase (GGT)

A

More sensitive than ALP for cholestasis in cats

Corticosteroids in dogs

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26
Q

What are some indicators of failure of hepatic synthesis and homeostasis

A

Urea- low if liver can’t convert NH3 to urea
Albumin- low if there is failure of synthesis but other causes too
Glucose- severe loss of functional mass the liver can’t maintain homeostasis
Cholesterol- hypo with hepatopathies and hyper with cholestasis

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27
Q

Is there any significance of having bile acids in serum

A

Bile acids normally resorbed from the ileum and under go recirculation so if there is bile acids in the blood there is a liver problem except in the presence of cholestasis

28
Q

Is it safe to perform a liver biopsy or FNA in a patient with suspected liver disease

A

If you think the animal is able to handle an anaesthesia and a coagulopathy test is done first
If in cats an ex lap is preferred so that you can have access to and biopsy multiple sites such as pancreas and SI

29
Q

What are the common hepatobilliary diseases of the dog and cat

A

Dog- Chronic parenchymal and portal hypertension

Cat- primary biliary disease and more resistant to setroids

30
Q

What does chronic hepatitis involve and what species affected most

A

Rarely causes icterus so diagnosed late stages
Young to middle aged dogs mostly affected
Mostly idiopathic but can have infectious or toxin cause
Portal hypertension as a result of inflam and fibrosis
Clinical signs start to appear once 75% of mass lost

31
Q

What are the clinical signs and diagnosis options for chronic hepatitis

A
Ascities develops due to hypertension
If icterus develops, poor prognosis
HE also develops at late stage
Peristently elevated ALT
Coagulation tests and wedge biopsy is definitive
32
Q

What are the management goals for a dog suffering from chronic hepatitis

A

ID and address underlying cause
Slow progression of disease
Supportive liver function- high quality and digestible protein
+/- antibiotics and glucocorticoids depending on biopsy

33
Q

Can dogs suffer from acute hepatitis

A

Yes, but it is rare
Can be caused by CAV-1, Panadol, heat stroke ect
Acute onset, high liver enzymes
Supportive care with IV fluids and good diet
If they survive the initial insult, liver has good regenerative capacity

34
Q

What are the two types of portosystemic shunts and are they more common in dogs or cats

A

Dogs
Congenital- diverts blood away from the liver
Shunting associated with portal hypertension to try and relieve some pressure

35
Q

What are some features of a portosystemic shunt in a dog

A
Poor growth and BCS
Neuro signs
Other congenital defects and unable to handle anaesthetic
Ultrasound is good but CT is better
Surgery is the best option
36
Q

Are primary or secondary liver diseases most common in dogs

A

Secondary are more common
Must exclude primary liver disease
Hepatic vacuolation- accumulation of glycogen or fat
Hepatic congestion and oedema- CHF

37
Q

What is the difference between primary and secondary hepatic lipidosis in a cat

A

Primary- massive accumulation of fat in hepatocytes leading to loss of function (obese cats)
Secondary- occurs in any anorexic cat with concurrent disease

38
Q

What are some clinical signs and diagnostic tools used in a cat with suspected hepatic lipidosis

A

Middle aged cat with recent stress or concurrent disease
Icterus, hepatomegaly, HE and coagulopathies common
Diagnosis reflects cholestasis with high ALT, AST and GGT, low urea, biopsy needed for definitive diagnosis
On radiographs there is weight loss but falciform fat remains
Cats normally too sick for anaesthesia to do biopsy

39
Q

What is the treatment available for hepatic lipidosis

A

Early and intensive feeding of high protein diet (1/4RER)
Probably will need to tube them to get them eating
IV fluids and antioxidants: S-adenosylmethionine

40
Q

What structures does triaditis include

A

Biliary disease + pancreas + duodenum

Hard to diagnose because signs are nonspecific

41
Q

What causes Neutrophilic (Suppurative) Cholangitis and how can it be diagnosed and treated

A

Ascending bacterial infection from SI
Triaditis, presents acutely in young-mid aged cats
High ALT and bilirubin but not sensitive or specific
Take a swab and MC&S of bile
Antibiotics for 4-6wks
IV fluids and tube feeding with ursodeoxycholic acid

42
Q

What is the most common cause of extrahepatic bile duct obstruction

A

Triaditis and neoplasia is second most common
Ultrasound reveals distended biliary tree
Treatment depends on what the underlying cause is
Try choleretics
Surgery doesn’t normally go well so avoid if possible

43
Q

Why is haemoabdomen a common finding in cats with hepatic amyloidosis

A

Liver is weak and easily damaged

No treatment and poor porgnosis

44
Q

What are the 4 general classes of therapy for an animal with liver disease

A

IV fluids- perfusion of damaged liver is important
Antibiotics- used in most cases
Antiemetics and gastric protectants- most feel nauseated
Analgesia- use opioid but not morphine > nausea

45
Q

What are some liver specific medications and what is there action

A

Ursodeoxycholic acid- hepatoprotective, choluretic and cholesterol reducing effects
S-adenosyl methionine (SAMe)- use drug because liver cant make its own and its important
Vit E- liver antioxidant, used with SAMe
Milk thistle- antioxidant and metabolic effects

46
Q

What are some important aspects of nutritional management of liver diseaes

A

Cats- get them eating or tube them
Feed a high protein that is highly digestible to stop tissue catabolism and nitrogenous waste
If the gut works, USE IT

47
Q

What are the 4 things that cats must be supplemented with

A

Thiamine
Cobalamin
L-carnitine
Taurine

48
Q

How do you deal with a dog in acute HE crisis

A
Emergency!
Remove or treat precipitating factors
IV fluid
Remove ammonia from colon with enema
IV ampicillin
Manage seizure with propofol or phenobarbitone
49
Q

How do you manage portal hypertension and ascities and what things should you avoid

A

Omeprazole to stop any GI bleeding and vitamin K if needed
If you need to give fluids, give colloid so it stays in vessels and doesn’t leak into abdo
Only give frusemide if animal cant breathe due to ascities
Avoid ulcerogenic drugs, sepsis, protein-calorie malnutrition

50
Q

How do you manage a coagulopathy as a result of liver disease

A

Coagulopathies common in liver disease

Provide parenteral vitamin K or fresh frozen plasma

51
Q

What is the one telling sign of Exocrine Pancreatic Insufficiency (EPI)?

A

There is always something wrong with the faeces

52
Q

What are the mechanisms behind EPI and what is normally present with EPI

A

Pancreatic acinar atrophy- autoimmune disease that attacks acinar cells but not islets (young adults)
Secondary to pancreatitis- major cause in cats, islet destruction and diabetes mellitus
SI bacterial overgrowth normally seen

53
Q

What is the pathogenesis of EPI

A

Lack of pancreatic digestive enzyme leads to maldigestion, bacterial overgrowth, malnutrition and weight loss but good appetitie
Vit B 12 def causes villous atrophy and further loss of digestion

54
Q

What are some clinical signs and treatment of EPI

A

Chronic steatorrhea
Seborrhea- essential fatty acid def
Cats- triadidtis

55
Q

How are you able to diagnose EPI

A

CBC, biochem and urine often normal- maybe PLE

TEST OF CHOICE- trypsin-like immunoreactivity (TLI)

56
Q

Are you able to treat EPI? If so, how?

A

Pancreatic enzyme supplementation for life
Available as powders or capsule or fresh raw cow pancreas, moderate fat and highly digestible diet
SIBO is assumed and treated with tylosin or metronidazole
2 or more meals a day to be fed
Good prognosis with owner compliance

57
Q

What is the pathophysiology of chronic pancreatitis

A

Destruction of pancreatic parenchyma
Autoimmune chronic- cocker spaniel
Idiopathic chronic- most common form

58
Q

What are some clinical features of chronic pancreatitis in dogs

A

Mild, intermittent GI signs
Acute pancreatitis episode > EPI
may cause extra-hepatic biliary obstruction

59
Q

What are some clinical features of chronic pancreatitis in cats

A

Mild and non-specific signs

Assoc with concurrent disease

60
Q

How are you able to diagnose a suspected case of chronic pancreatitis

A

Biopsy is the only definitive test but not commonly done because confirmation won’t change treatment
cPLI most sensitive for dogs but only shows up in acute flare ups
Treatment is symptomatic only or treated acutely

61
Q

Why doesn’t the pancreas digest itself

A

Trypsin is stored in an inactive form called trypsinogen

The pancreas also releases a trypsin inhibitor

62
Q

What is the aetiopathogenesis in acute pancreatitis

A

Premature activation of trypsin causing autodigestion and activation of other enzymes
Autodigestion- multifactorial
90% of cases are idiopathic

63
Q

What are some clinical features of acute pancreatitis in dogs

A

History of high fat meal or over eating

Look for a position of relief, looks like GI obstruction

64
Q

What are some clinical features of acute pancreatitis in cats

A

Concurrent features of other diseases

May have LI diarrhoea and develop icterus

65
Q

What are some things you expect to find in a clinical exam of an acute pancreatitis animal

A

Shock
Pain on palpation of abdomen and a mass
Concurrent endocrine disease

66
Q

How are you going to diagnose a case of acute pancreatitis

A

cPLI/fPLI- don’t know if it has prognostic implications
Best test to use
US better than x-ray- enlarged hypoechoic pancreas with hyperechoic surrounding fat

67
Q

How can you treat a case of acute pancreatitis

A

IV fluids and electrolytes- 90mL/kg/hr for 30mins 4 shock
Nutritional support- enteral nutrition as early as possible
Analgesia- butorphanol or methadone if bad pain
Antiemetics- maropitant
Antibiotics if indicated- enrofloxacin + metronidazole