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VET377B SPAM Second Half > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

What does an increase in AST indicate?

A

Liver or Muscle damage. Must do CK to determine if muscle is involved

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2
Q

What does an increase in Alk Phos and GGT indicate?

A

Cholestasis

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3
Q

What are some specific signs of hepatic disease?

A
  • Hepatomegaly
  • Microhepatica
  • Icterus
  • Ascities
  • Hepatoencephalopathy
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4
Q

What are the 2 categories of Hepatic Enzymes?

A

Hepatocellular Leakage Enzymes (indicates hepatocellular damage) Induced Enzymes

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5
Q

What are the Hepatocellular Leakage Enzymes?

A
  • Alanine Aminiotransferase (ALT)
  • Aspartate Aminotransferase (AST)
  • Sorbitol Dehydrogenase (SDH)
  • Glutamate Dehydrogenase (GLDH)
  • Ornithine Carbamyltransferase (OCT)
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6
Q

Where is the highest activities of ALT found?

A

In hepatocytes and striated (Skeletal and Cardiac) Muscle Cells

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7
Q

Whats the difference between Horses and Dogs & Cats when talking ALT?

A

In Horses ALT is generally from Muscle In Dogs & Cats its from Liver.

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8
Q

If we lose 75% of the functional mass of our liver what Biochem changes would we see? (Decreased Functional Hepatic Mass)

A

Decrease in :-

  • Glucose
  • Urea
  • Albumin
  • Cholesterol
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9
Q

What is the halflife of ALT in a dog?

What is the half life of ALT in a Cat?

A

Dog 60 Hours (2-3days)

Less than 24hours in a Cat

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10
Q

What is the half life of Alk Phos in a dog?

A

About 3 days

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11
Q

If our Urea is slightly high and our Creatinine is normal what would we need to do next?

A

Do a SG to determine if the azotemia is pre-renal or primary renal.

Concentrated SG = Pre-renal

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12
Q

What are some non-specific clinical signs of Hepatic disease?

A
  • Depression
  • Weight Loss
  • Anorexia
  • Vomiting
  • Abdominal Pain
  • PU/PD
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13
Q

What are some tests we can do to test for liver disease

A
  • CBC
  • Serum Biochemistry
  • Tests of Liver function
  • Urine Sample
  • Liver Biopsy
  • Abdominal imaging
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14
Q

What is this cell?

A

Leptocyte

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15
Q

What is the name of this RBC

A

Schistocyte

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16
Q

If a Serum biochem results showed a Hyperbilirubinaemia what would your differentials be?

A
  • Hyperbilirubinaemia
    • Haemolytic Disease
    • Decreased hepatic functional mass
    • Cholestasis
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17
Q

In Dogs and Cats what is ALT considered to be specific for?

A

Hepatic Injury

It will also increase with SEVERE muscle injury

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18
Q

After initial liver damage when does serum ALT activity :-

  • First increase seen?
  • Peaks?
  • Returns to the reference range?
A
  • 12hours after injury
  • 1-2days
  • 2-3weeks
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19
Q
  • What is an increase in AST (Aspartate Aminotransferase) indicate?
  • How do you differentiate between the locations that AST has come from?
A
  • Acute or Chronic liver injury
    • Muscle damage in all domestic species
  • Run a CK concurrently to differentiate between AST from muscle and liver.
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20
Q

What is the half life of AST in the :-

Dog

Horse

A
  • Dog = 12 hours
  • Horse = 6-7days
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21
Q

Which test will indicate Liver/Biliary damage?

A
  • Hepatocellular leakage
    • ALT
    • AST
    • SDH
    • GLDH
    • OCT
  • Induced enzymes
    • ALP - Alkaline Phosphatase (AlkPhos)
    • GGT - Gamma Glytamyl transferase (GGT)
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22
Q

How do you differentiate between acute and an ongoing disease process of the liver?

A

Doing AST/ALT testing a few days apart

23
Q

What tests would you do to measure hepatic synthetic capability?

A
  • Albumin
  • Urea
  • Cholesterol
  • Glucose
  • Clotting Times
24
Q

What of the liver leakage enzymes do we check in Horses, Sheep, goats and cows for detecting hepatocellular damage?

A

SDH - Sorbitol Dehydrogenase

25
Q

What are the Liver Induced enzymes?

A

Alkaline Phosphatase (ALP)(Alk Phos)

Gamma Glytamyl Transferase (GGT)

26
Q

What does an increase in ALP activity indicate?

A

Cholestasis

PS. Only increases of ALP are of significance decreases are not

27
Q

Outline Bilirubin metabolism and excreation

A
  • Extravascular or intravascular hemolysis of RBC, Haemoglobin broken into Haem and Globin -
  • Unconjugated bilirubin + albumin heads to the Liver wher it becomes CONJUGATED BILIRUBIN
  • Through the billiary system into the small intestine where bacterial proteases convert it into Urolibinogen
  • 10% of this Urolibinogen is reabsorbed and taken up via the portal vein. The remaining 90% is eliminated in fecaes
  • The Urobilinogen that is now in the blood is then filtered out in the kidney and excreted in urine.
28
Q

What can Hyperbilirubinaemia be caused by?

A
  • Increased destruction of RBC (Pre-Hepatic) - Unconjugated
  • Hepatocellular dysfunction (Hepatic) - Mixed
  • Cholestasis (Post-hepatic) - Conjugated
29
Q

What would we see in a horse that is inappetent or decreased feed intake?

A

The horse could be jaundice and have an increase of plasma biliruben due to the decrease in hepatic up-take and conjugation of biliruben by the liver.

It rapidly resolves following the resolution of the anorexia or an infusion of glucose.

30
Q

Bile Acids

Where are Bile acids synthesised?

WHat is their function?

how are the secreted?

A
  • Bile Acids are Synthesised in the liver from cholestrol
  • The Function of Bile Acids are to solubilise lipids and aid in fat digestion.
  • Conjugated and secreted into the Bile
31
Q
  • How do we test for Bile Acids?
  • What can an Increased Bile Acids result be cause by?
A
  • Measure of bile acids in paired (Fastin and 2hr post-prandial samples
  • Increased Bile Acid Causes
    • Porto-systemic Shunt
    • Liver Failure
    • Cholestasis
    • Inappropriate contraction of the gall bladder
    • SIBO (Small Instestine Bacterial Overgrowth)
32
Q

What is the upper limit of fasting Bile Acid concentration for Dogs and Cats?

A

Dogs > 30

Cats >25

33
Q

How is ammonia produced an metabolised within the body?

A
  • Produced inthe GIT by breakdown of Amino Acids and urea by microflora
  • Transported to liver via portal circulation
  • Converted to Urea via urea cycle in the liver
  • Excreated in Urine
34
Q

Why would we see Ammonium bi-urate crystals in urine?

A
  • Normal finding in Dalmations
  • Often seen when there is increased blood ammonia levels
35
Q

If we suspect liver insufficency what would you test for to see?

A

You would see a decrease in :-

Urea

Ammonia

Glucose

Albumin

Clotting Times

36
Q

What cells make up the liver?

A
  • Hepatocytes
  • Endothelial Cells
  • Kupffer Cells
  • Biliary Epithelial cells
  • Hepatic Stellate cells
37
Q

What are the normal liver functions?

A
  • Bilirubin/Bile acid metabolism
    • Excretion and conduction of bile
  • Carbohydrate and lipid metabolism
    • gluconegenesis/glycolysis and ketogenesis
  • Xenobiotic metabolism
    • Especially via cytochrome p450 enzyme system
  • Protein synthesis
    • Albumin, clotting factors, acute phase proteins
    • Also principal site of ammonia metabolism
  • Immune Function
38
Q

What is Bile for?

How is it conducted and excreted?

A
  • Important for digestion of fats (Bile acids) and for elimiation of wastes (eg. Bilirubin)
  • Excreted into canaliculi –> intralobular bile ducts (Canals of hering –> interlobular bile ducts –> hepatic ducts –> gallbladder (when present) via cystic duct –?> common bile duct –> duodenum
39
Q

What are some consequences of liver dysfunction?

A
  • Disturbances of bilirubin excretion/secretion
    • Cholestasis –> icterus/jaundice, hyperbilirubinuria
  • Inadequate conversion of ammonia to urea
    • Increased ammonia, decreased urea, hepatic encephalopathy
  • Defects in protein synthesis
    • Hypoalbuminaemia, decreased clotting factors (coagulopathy)
  • Abnormal carbohydrate and fat metabolism
    • usually hypoglycemia
    • May see decreased cholesterol, hepatic lipidosis
  • Aquired portosystemic shunting
    • hepatic encephalopathy
  • Portal Hypertension
    • Ascites
  • Abnormal metabolism of chlorophyll
    • Secondary (type III) photosensitisation (Herbivours)
  • Failure of Kupffer cell activity
    • Can lead to increased bacteria entering circulation
  • Altered metabolism of drugs and chemicals
40
Q

What is the functional reserve of the liver?

A

70-75%

41
Q

What are some clinical signs of hepatic disease?

A
  • Lethargy/malaise/ill thrift/depression
  • Abdominal distension (Ascites, hepatomegaly)
  • CNS signs (hepatic encephalopathy)
  • Inappetance/anorexia
  • Vomitins and/diarrhoea
  • Jaundice and dark urine
  • Abdominal Pain
  • Weight Loss
  • secondary Haemostatic disorders
  • Photosensitisation
  • Drug intolerance
42
Q

What is Jaundice?

What are the 3 subcategories of causes of Jaundice?

A
  • Hepatic injury frequesntly manifests as increased bilirubin in the blood (hyperbilirubinaemia)
  • High concentrations leads to yellow staining of the tissue by bilirubin = jaundice (Icterus)
  • Pre-hepatic
  • Hepatic
  • Post-hepatic
43
Q

Of the 3 categories of Jaundice give an example of each and give the mechanism

A
  • Pre-Hepatic
    • Due to increased RBC destruction (Haemolysis)
      • IMHA, Infectious (rickettsia) Metabolic
      • Increased unconjugated (at first)
  • Hepatic
    • Due to liver disease
      • Any disease compromising the livers ability to uptake conjagate, and/or secrete bilirubin
      • Usually severe, difuse hepatic disease eg cirrhosis, widespread acute HC degeneration/necrosis
      • Increased unconjugated and conjugated bilirubin
  • Post-Hepatic Jaundice
    • Due to bile duct obstruction eg pancreatitis, choleliths
      • Increased conjugated bilirubin
44
Q

What are the main portals of entry by which pathogens gain access to the liver?

A
  • Haematogenous
  • Biliary
  • Direct Penetration
45
Q

What are the 3 patterns of acute degeneration/necrosis of the liver?

A
  1. Random hepatocellular degeneration/necrosis
    • Typically an infectious agent eg bacteria, viruses (herpes), protozoa
  2. Zonal hepatocellular degeneration/necrosis
  3. Massive Necrosis (and submassive)
46
Q

What are the 5 zonal patterns of hepatocellular degeneratoin/necrosis?

A
  1. Centrilobular degeneration/necrosis (periacinar)
  2. Paracentral degeneration/necrosis
    • Affects apex of acinus (wedge shaped around central vein)
  3. Midzonal degeneration/necrosis
  4. Periportal degeneration/necrosis
  5. Bridging degeneration/necrosis
47
Q

What would the likely cause of Acute Hepatitis be?

A
  • Usually infectious and part of systemic infection
    • Viral : Herpesvirus, Canine infectious hepatitis (CAV-1), FIP
    • Bacterial : Salmonellosis
    • Parasitic : Toxoplasma godii
    • Fungi : Zygomycetes
  • Often multifocal random
  • Inflammation
    • Neutrophils dominate, fibrin, +/- lymphocytes if viral, can lead to abscessation
  • Hepatocellular necrosis
48
Q

What are some examples of Acute Hepatic Disease

A
  • Herpesvirus
  • Canine infectious hepatitis (Canine adenovirus 1 CAV-1)
  • Campylobacteriosis
  • Hepatosis dietecia
49
Q

What are the livers responce to injury?

A
  • Regeneration
    • Mild to moderate single incident sublethal injury may result in full regeneration and full restoration of function
  • Fibrosis
    • Repeated bouts of low-level sublethal injury injury or severe, single incident injury can initiate hepatic fibrosis and nodular hepatocellular regneratio - this can lead to progressively worsening fibrosis which eventually bridges across the lobule/between lobules and may progress to cirrhosis
  • Biliary hyperplasia
    • Non-specific responce to a variety of insults, particularly prominent with biliary obstruction
50
Q

Define Cirrhosis

A
  • A diffuse process characterised by fibrosis and conversion of the normal liver architecture into structurally abnormal lobules
51
Q

List the clinical signs for:-

Acute liver failure

Chronic Liver Failure

A
  • Acute Liver Failure
    • ​Early CS
      • Dullness, depression, neurologic manifestation (hepatic encephalopathy)
      • Vomiting, abdominal pain
      • Weakenss (Hypoglycaemia)
      • PU/PD, bilirubinuria
      • Secondary haemostatic disorders +/- DIC
      • Bilirubinaemia/bilirubinuria
    • Late CS
      • Icterus
      • Hepatic encephalopathy
  • Chronic Liver failure
    • Hypoalbuminaemia
    • Portal hypertension –> ascites
    • Acquired portosystemic shunts
    • Cutaneous lesions - hepatocutaneous syndrome in dogs and photosensitisation in herbivores
    • Imparement of immune function –> endotoxaemia/systemic infection
52
Q

What is Cholestasis?

What are the 2 types of Cholestasis?

A
  • Suppression of bile production/bile flow
  • Intrahepatic (Most common)
    • decreased ability of Hepatocytes to metabolise/excrete bile (injury/congenital)
    • HC swelling –> compresses and blocks canaliculi
    • Inflammation +/- necrosis of bile ductules
  • Extrahepatic
    • ​Due to blockage of extrahepatic bile ducts
    • Intraluminal choleliths/parasites
    • Extraluminal pressure (adjecent neoplasia, inflammation eg pancreatitis)
53
Q

What are the 3 stages of Chronic Copper Toxicosis:Sheep?

A
  • Slow hepatic copper accumulation within lysosomes due to :
    • Excess dietary intake, low molybdenum/ sulfur pastures or pre-sensitisation due to pasture containing hepatotoxic phytotoxins
  • Hepatocellular damage
  • Haemolytic Crisis
    • Stressful event triggers sudden release of coppor into blood –> triggers acute, severe intravascular haemolysis –> anaemia –> extensive centrilobular hepatocellular necrosis due to tissue hypoxia

VET377B SPAM Second Half (7 decks)

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