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Year 4 > SA Liver > Flashcards

SA Liver Flashcards

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1
Q

When may ammonia be raised?

A

Liver failure

Congenital and acquired portosystemic shunts

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2
Q

How may urine be affected by liver disease?

A

Isosthenuria or inappropriately low USG
Bilirubinuria
Ammonium biurate crystals or uroliths

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3
Q

When investigating liver function, what can we test?

A

Hepatocellular injury
Cholestasis
Hepatocellular function
Hepatic portal circulation

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4
Q

Where are enzymes mostly found?

A

Inside cells (no function in blood)

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5
Q

How are proteases stored?

A

As inactive zymogens

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6
Q

Give 5 changes that indicate reduced hepatocellular function

A

Decreased uptake and excretion of bilirubin and bile acids
Decreased conversion of ammonia to urea
Decreased synthesis of metabolites
Decreased synthesis of coagulation proteins
Decreased immunologic function

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7
Q

Which enzymes are produced by pancreatic acinar cells?

What else do they produce?

A

Proteases (trypsin, chymotrypsin, elastase)
Lipases
Amylase

Also bicarbonate

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8
Q

Give some other functions of pancreatic enzymes

A

Proteases aid B12 absorption
Aid zinc absorption
Antibacterial activity
Intestinal mucosal modulation

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9
Q

What tests can we carry out to test exocrine pancreatic function?

A 
Enzyme assays for amylase and lipase (poor specificity)
DGGR lipase (more specific)
'Specific' canine pancreatic lipase (cPL) (more specific and sensitive than lipase and amylase) (Test available at external labs or in-house SNAP tests)
TLI (trypsin-like immunoreactivity) (not as sensitive as cPL)
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10
Q

What is the function of amylase?

Why may it be increased?

A

Catalyses hydrolysis of complex starches

Can increase due to decreased GFR

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11
Q

What is the function of lipase?

Why may it be increased?

A 
Catalyses hydrolysis of triglycerides 
Can increase (mildly) due to decreased GFR
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12
Q

When testing DGGR lipase, what are the cut-off values for diagnosis of pancreatitis?

A

> 34 U/L in cats

>216 U/L in dogs

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13
Q

After finding an elevation in lipase, what tests would you carry out to confirm a diagnosis of pancreatitis?

A

PLI (specific pancreatic lipase)
Imaging (ultrasound)
Biopsy
Fluid analysis

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14
Q

When would you test for TLI (trypsin-like immunoreactivity)?

A

In animals with clinical signs of maldigestion/malabsorption
High sensitivity/specificity for exocrine pancreatic insufficiency
Less useful for pancreatitis

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15
Q

What does a TLI test detect?

A

Trypsin, trypsinogen, and trypsin bound to protease inhibitors (most TLI in blood is trypsinogen, do not want free trypsin in the blood)

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16
Q

What value of cPL (specific canine pancreatic lipase) indicates pancreatitis?

A

> 400ug/L

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17
Q

Which cells are present in the pancreas?

A 
PP cells (produce pancreatic polypeptides)
B cells (produce insulin)
Delta cells (produce somatostatin)
Alpha cells (produce glucagon)
Acinar cells (produce digestive enzymes)
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18
Q

What can we test to investigate liver function?

A

Hepatocellular injury (damage to hepatocytes -> leakage of enzymes)
Cholestasis (reduced/blocked bile excretion -> release of enzymes induced by retained bile)
Hepatocellular function (decreased production/catabolism of substances)
Hepatic portal circulation (decreased extraction of substances absorbed from the GI)

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19
Q

In which case may increased AST be artefactual?

A

Leakage from RBCs

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20
Q

Which are the liver ‘leakage’ enzymes?

A

ALT (largely liver-specific but also muscle. SA)
AST and LDH (both liver and muscle)
SDH and GLDH (liver specific in all species. Used in LA)

ALP and GGT are indicative of liver damage in horses and ruminants

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21
Q

What is cholestasis?

A

Decreased bile flow and excretion

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22
Q

What are the 3 kinds of cholestasis?

A

Intrahepatic (due to hepatocellular swelling)
Extrahepatic (due to bile duct obstruction)
Functional (nothing mechanically abnormal)

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23
Q

What can you use as markers for cholestasis?

A

Bilirubin
Bile acids (more sensitive)
Cholesterol
ALP and GGT (cholestatic enzymes; GGT is more specific)

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24
Q

What are the 2 major isoforms of ALP?

A

Liver-ALP (L-ALP)

Bone-ALP (B-ALP)

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25
C-ALP is induced by what? | In which species?
Corticosteroids | Dogs
26
Where is haem broken down to bilirubin?
Macrophages
27
What is bilirubin conjugated with in the liver?
Glucoronic acid
28
What are the 3 types of hyperbilirubinaemia?
Pre-hepatic: secondary to haemolysis of RBCs Hepatic: due to decreased bilirubin uptake, conjugation, and excretion. Often due to concurrent hepatocyte dysfunction and intra-hepatic cholestasis Post-hepatic: Secondary to obstruction of extra-hepatic bile duct
29
Does conjugated or unconjugated bilirubin predominate with pre-hepatic bilirubinaemia?
Unconjugated at first, then an increasing proprotion of conjugated as time passes Also, some degree of cholestasis
30
Does conjugated or unconjugated bilirubin predominate with post-hepatic bilirubinaemia?
Conjugated
31
Why may jaundice persist long after liver function has returned to normal?
Due to delta-bilirubin, bound to albumin | Will be no bilirubinuria
32
Give some functions of the liver
Removal of bacteria Produces clotting factors Storage of glycogen, iron, copper and vitamins Detoxification of body wastes, drugs, and xenobiotics Synthesis of cholesterol and bile acids Synthesis of plasma proteins Breakdown of RBCs Carbohydrate, lipid and amino acid metabolism
33
What produces bile acids?
Hepatocytes
34
Describe the route of bile acids
Produced by hepatocytes Released into biliary system then intestine Over 90% are reabsorbed from the ileum, enter portal vein, return to liver, recirculated Small amount lost in faeces; replaced by liver
35
Why may bile acids be increased?
Reduced uptake/excretion by hepatocytes (reduced hepatocyte mass/function) Disruption of enterohepatic circulation (portosystemic shunts, cholestasis)
36
Which value for bile acid concentration indicates increased production and hepatobiliary pathology?
Values >25-30 mmol/L
37
How can you test for post-prandial SBA?
``` (Post-prandial serum bile acids) Take resting sample Fatty meal Post-prandial sample 2 hours after feeding If >25-30 mmol/L -> abnormal ```
38
What is meant by a 'reactive hepatopathy'?
Many extrahepatic diseases cause elevation in liver enzymes | eg hypoxia, GI and pancreatic disease, sepsis
39
What haematology may we see in liver disease?
Often unremarkable but we may see: Acanthocytes Microcytosis Ovalocytes (cats with hepatic lipidosis)
40
What are the 3 cholestatic markers?
Bilirubin, GGT, ALP
41
What must you always do before taking a liver biopsy?
Check clotting profile | Liver makes clotting factors-impaired liver function may result in reduced clotting factors
42
Where does the liver get its blood supply?
``` Hepatic portal vein (70-80%) Hepatic artery (20-30%) ```
43
What are the 3 major types of icterus
Pre-hepatic (haemolysis) Hepatic (hepatocyte dysfunction, intrahepatic cholestasis) Post-hepatic (extra-hepatic cholestasis)
44
Give some clinical signs of metabolic dysfunction
Non-specific signs (loss of condition, weight loss) Hypoglycaemia (can cause seizures/collapse) Hypoalbuminaemia (only in chronic disease; can contribute to ascites)
45
What do copper-coloured irises indicate in cats?
Portosystemic shunt
46
Give some circulatory disturbances caused by liver disease
Ascites PUPD Portosystemic shunts
47
How do hepatic encephalopathies occur?
Liver is unable to turn NH3 into urea (decreased functional liver mass and/or portosystemic shunt) Increased blood NH3 (plus other toxins) Leads to altered CNS function
48
Give some CNS signs seen with hepatic encephalopathies
Anorexia, vomiting and diarrhoea, PUPD | Dullness, aggression, staggering, blindness, head-pressing, seizures
49
When are hepatic encephalopathies worse?
After a high protein meal GI bleed Dehydration, acid-base imbalance
50
Why is bleeding seen with liver disease?
Defective production and storage of clotting factors Vitamin K malabsorption Portal hypertension -> GI bleeding
51
Give some clinical signs of a portosystemic shunt
``` Ascites Stunted growth (if young) Vomiting and diarrhoea PUPD Non-specific signs (anorexia, weight loss, weakness, poor coat and skin condition) ```
52
How can we classify hepatopathies?
Primary (inflammatory or non-inflammatory) | Secondary
53
Give some causes of reactive hepatopathies
``` IBD Bacterial infections Periodontal disease (can cause bacteraemia) Riskettsial infections Acute pancreatitis Diabetes mellitus Hyper/hypoadrenocorticism R-HF Hyperthyroidism Septicaemia ```
54
Give some bacterial causes of an inflammatory, infectious hepatopathy
``` Leptospirois Bacterial cholangiohepatitis (ascending infection from intestines) ```
55
Give some viral causes of an inflammatory, infectious hepatopathy
Infectious canine hepatitis Canine herpes virus FIP
56
Give a protozoal cause of an inflammatory, infectious hepatopathy
Toxoplasma
57
Give some causes of an inflammatory, non-infectious hepatopathy
Toxic hepatic disease Drug-induced hepatic disease All forms of chronic hepatitis (canine chronic hepatitis, feline lymphocytic cholangitis)
58
Give some causes of a non-inflammatory hepatopathy
``` Congenital portosystemic shunt Juvenile hepatic fibrosis Feline hepatic lipidosis (rare) Neoplasia Telangiectasia (permanent dilation of blood vessels) and peliosis (blood-filled cavities throughout liver) -> fragile liver Surgical: trauma, liver lobe torsion Amyloidosis ```
59
Which enzyme are cats deficient in which makes them more sensitive to certain toxins/drugs?
Glucuronyl transferase (results in difficulty conjugating toxins)
60
How does paracetamol toxicity occur in cats?
Deficient in glucuronyl transferase therefore deficiency of glucuronidation Results in methaemoglobinaemia -> haemolytic anaemia, facial oedema, hepatocellular damage (liver failure and icterus)
61
What is the treatment for paracetamol poisoning in cats?
N-acetlycysteine S-adenosyl methionine Vitamin C Supportive care: ABs, IV fluids, activated charcoal if recent ingestion
62
Give some differentials for icterus in cats, starting with the most common (*)
*Cholangitis complex *FIP (dry form) *Lymphoma *Lipidosis *Pancreatitis Cirrhosis Neoplasia Toxoplasmosis Haemolytic anaemia Toxic hepatopathy Panleucopenia Biliary obstruction/ bile duct rupture
63
What will you see first- an increase in serum bilirubin or visible icterus?
Increase in serum bilirubin
64
What is microhepatica a sign of?
Portosystemic shunt
65
What should you always do before taking a liver biopsy?
Coagulation tests/check clotting profile
66
What do liver enzyme tests tell you?
If liver is affected by something, NOT if its function is impaired
67
Which liver enzymes can you test?
Hepatocellular markers: ALT, AST | Cholestatic markers: ALP, GGT
68
Which liver function tests can you do?
``` Bile acids (most sensitive) Serum proteins (esp. albumin) Glucose, urea, cholesterol (produced in liver) Bilirubin Ammonia ```
69
What do you see first with chronic hepatitis: altered lab results or clinical signs?
Altered lab results
70
When might you typically do a portovenogram?
Looking for a portosystemic shunt
71
What can you look at on a radiograph to give you an idea of liver size?
Position of gastric axis
72
What is the best way to diagnose most liver conditions?
Liver biopsy
73
Give some indications for a liver biopsy
Persistent increase in liver enzymes Altered liver size Monitoring progressive liver disease To evaluate response to treatment
74
How can you perform a liver biopsy?
Percutaneous (blind; US-guided with 'Tru-cut') Laparoscopy Coeliotomy
75
Give some contraindications for doing a percutaneous liver biopsy
``` Lack of operator experience Small liver (unless US-guided) Focal disease (easy to miss) Extrahepatic cholestasis Bleeding disorder Severe anaemia ```
76
Which dog breeds are more prone to juvenile hepatic fibrosis?
GSD, Rottweiler
77
Describe the pathology of juvenile hepatic fibrosis
- Progressive fibrosis - Minimal inflammatory reaction - Central vein fibrosis and occlusion most common
78
How do acquired shunts occur?
Secondary to liver disease (juvenile hepatic fibrosis, cirrhosis)
79
Where do acquired shunts develop?
From redundant vessels (between portal vein and caudal vena cava)
80
Which clinical sign is often seen with acquired portosystemic shunts but rarely congenital?
Ascites
81
What is the most common canine chronic liver disease?
Canine chronic hepatitis
82
Give some types of canine chronic hepatitis | What may they all lead to?
-Idiopathic chronic hepatitis -Lobular dissecting hepatitis -Drug-induced chronic hepatitis -Copper-associated hepatitis May all lead to cirrhosis
83
Which 3 factors may lead to a shorter survival time for canine chronic hepatitis?
Hypoalbuminaemia Severe necrosis and fibrosis in biopsy Bridging fibrosis
84
What is cirrhosis?
Shrunken liver from fibrosis (micro/macro-nodular regeneration) End-stage of many diseases
85
Which breeds are more affected by hepatic portal hypoplasia?
Small terrier breeds
86
What makes up feline cholangitis complex?
- Suppurative cholangitis (neutrophils) - Lymphocytic cholangitis (lymphyocytes and plasma cells; indicates immune-mediated) - (Sclerosing cholangitis- end stage of others) - Can get both in combination with IBD and pancreatitis
87
What does idiopathic hepatic lipidosis lead to?
Biliary stasis Liver failure Anorexia Death
88
Give some examples of primary liver tumours
``` Hepatocellular carcinoma Hepatoma Cholangiocarcinoma Fibroma/sarcoma Haemangioma/haemangiosaecoma ```
89
How do you treat hepatic encephalopathy?
Low protein diet Lactulose ABs (ampicillin or metronidazole)
90
How do you treat chronic active inflammation of the liver?
Glucocorticoids | Diet: low copper, high zinc, high protein quality, anti-oxidants. Taurine and L-carnitine for cats
91
Which liver conditions can you treat with glucocorticoids?
Chronic active inflammation | Hepatic fibrosis
92
Which dog breeds are affected by copper-associated hepatopathies?
``` WHWT Skye and Bedlington terrier Labrador Dalmation Doberman ```
93
Which agents are 'de-coppering agents'?
Copper chelators: D-penicillamine, Trientine (222-tetramine) | Copper absorption blocker: oral zinc
94
What is UDCA?
Ursodeoxycholic acid | Alters bile composition and stimulates bile flow (CI if complete biliary obstruction)
95
What is SAMe?
S-Adenosyl methionine | Precursor for GSH production (molecule central to hepatic metabolism and detoxification)
96
How do you treat bacterial cholangiohepatitis?
Do culture and sensitivity and give appropriate ABs
97
How do you treat an immune-mediated process in the liver?
Prednisolone +/- azathioprine
98
How do you treat liver fibrosis?
Prednisolone +/- alter the diet/ give UDCA (modulates immune response)
99
How do you treat copper accumulation?
Penicillamine, trientine, zinc
100
Give some complications of liver disease
Hepatic encephalopathy and coma Ascites and oedema Haemorrhage and anaemia
101
How can we treat ascites and oedema caused by liver disease?
Low sodium diet Diuretics (spironolactone) Paracentesis (only drain a minimal volume, as can worsen bodywide protein status)
102
Which two liver leakage enzymes indicate hepatocellular damage?
ALT (largely liver-specific) | AST (not liver-specific; also to muscle)
103
How would you identify cholestasis on cytology?
Presence of dark green-black granular pigment between hepatocytes
104
What in unconjugated bilirubin bound to in the blood?
Albumin
105
Which haematology changes might you see with liver disease?
Microcytosis (PPS or severe liver insufficiency, likely due to altered iron transport/metabolism) Ovalocytes/elliptocytes (cats with hepatic lipidosis) Acanthocytes (spiked cell membrane; lipid disorders, disruption of normal vasculature)
106
What may you see on a urinalysis of a pet with liver disease?
Isosthenuria or low SG Bilirubinuria (>2 in dogs, any in cats) Ammonium biurate crystals or uroliths (40-70% of patients with PSS)

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