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Lecture 18 Flashcards

1
Q

What is important about the liver

A

Subject to more toxins than any other organ as it is the portal blood flow directly from GIT

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2
Q

What are the two toxic effects

A
  1. Intrinsic: predictable toxic effect is given species and dose range
  2. Idisyncraric: less dose dependent and only seen in a small number of individuals
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3
Q

What does the severty of hepatotoxicty depend on

A
  1. Age, sex, diet, genetics, endocrine
  2. Dose
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4
Q

What are most hepatotoxins

A

Predictable (intrinsic)

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5
Q

What are cats deficient in

A

Glucaronyl transferase

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6
Q

Where are idiosyncreatic reations seen

A

Small number of individual animals

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7
Q

What are 4 things to consider with idiosyncratic reactions

A
  1. Atypical metabolism due to genetic variation in enxymes
  2. Atypical immune response
  3. Interactions with other drugs
  4. Most drugs need bioactivation in liver
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8
Q

What are the categories of Hepatotoxic injury

A
  1. Injurious intermediary metabolites produced by cytochrome P450 enxymes - substances activated in liver
  2. Alteration of cells to become antigenic to immune system - Drugs and cellular constituents combine form neoantigens
  3. Stmulation of apoptosis - direcof toxins or immune mediated
  4. Membrane damage and disruption to calcium homeostasis - calcium activates damaging enzymes such as proteases
  5. Mitochondrial damage - disrupt energy supply to cells - disrupt energy supply to cell
  6. Disruption of bile secretion causing cholestasis - interupt molecular pumps that secrete bile
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9
Q
A
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10
Q

Explain acute hepatotoxic injury

A

Within 2-3 days

  • Macrophages clear debris
  • Remainig hepatocyes withn lobule proliferation

One week later

  • Normalhistologic appearance
  • Unless massive necrosis

Marked to massive coagulatice centrilobular necrosis with haemorrhage, possible acute hepatic failure

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11
Q
A

Acute hepatotoxic injury

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12
Q

How do animals get chronic hepatotoxic injury

A

Repeated bouts of exposure or daily ingestion

  • Activation of stellate cells > fibrosis
  • Disruption of architecture
  • Nodules of regeneration
  • > Cirrhosis

When severe enough there is signs of hepatic failure

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13
Q

Clincial signs of acute hepatoxicty

A
  • Rapid death
  • Anorexia
  • Depressin
  • Colic
  • Seizures
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14
Q

Gross appearance of hepatotoxicity

A
  • Swollen/enlarged
  • Turgid/firable
  • Red-yellow mottled to dark purple
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15
Q

Clinical signs of chronic hepatotoxicity

A
  • Weight loss
  • Jaundice
  • Photosensitization
  • Head pressing, wandering
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16
Q

Gross appearance of chronic hepatotoxicity

A
  • Small
  • Pale tan to yellow
  • Firm
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17
Q

What do pyrrolizide alkaloids cause

A
  1. Toxins are metabolised to active form in liver
  2. Prevents cell division - but cells continue DNA synthesis
  3. Usually chronic toxicity
    1. Megalocytosis
    2. Fibrosis
    3. Biliary hyperplasia
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18
Q
A

Chronic Pyrroliidine alkaloid Hepatotoxicity: Fibrosis and Distortion

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19
Q
A

Chrinic Pyrrolizidine Alkaloid Hepatotoxicity: megalocytes, fibrosis, biliary hyperplasia

20
Q

How is lantana toxic

  • Subacute signs
  • Signs of liver failure
A
  • Damage bile canaliculi membrane -> Cholestasis
  • Subacute signs: signs within a few days (depression, dehydration, constipation)
  • Signs of liver failure
    • Jaundice
    • 2nd degree photosensitisation
    • Death 1-4 weeks
21
Q

Pathological changes seen with latana

A
  • Photosensitisation
  • Icterus
  • Swollen liver and kidneys
  • Distended gall bladder
  • Constipation
22
Q

What is the liver histopathology seen with lantana

A
  • Often mild chnages
  • Cholestasis
  • Hepatocyte swelling with fine vacuolation
  • Fibrosis and bile duct changes
23
Q

How are cycads and zamia plants toxic

A

Seeds contain cyasin/microzamin

  • Broken down in GIT by bacteria to MAM
  • Converted to active form by enzymes in the liver
24
Q

Where is acute intoxication with cycads and zamia seen and what does it cause

A

Sheep

  • Swollen red liver and acities
  • Centrolobular hepatic necrosis: GIT dysfunction
25
Where is chornic toxicity with cycads and zamia plams seen and what is the effect
Cattle * Hepatic necrosis and dissecting fibrosis
26
What produces aflatoxin
Product of fungus: Aspergillis flavus, A. parasiticus, Penicillium puberulum
27
Where is acute aflatoxosis usually seen and what does it cause
Dogs Haemorrhagic centrolobular to massive necrosis
28
What is seen with chronic alflatoxicosis
* Shrunken fibrotic liver * Fatty change, biliary hyperplasia, centrilobular fibrosis, metalocytosis
29
Chronic hepatic aflatoxicosis: fatty change and biliary hyperplasia
30
What is sporidesmin and its cause
Facial eczema​ * Product of fungus Pithomyces chartarum * Grows in moistened dead rye grass * Cause cholestasis and failure to ecvrete phylloerythrin
31
What is the gross pathology of Sporidesmin
* Secondary photosensitisation esp on face * Bile stained liver
32
What is the histopathology fo sporidesmin
* Cholangitis and cholestasis * Necrosis of biliary epithelium * Dilatele ducts
33
Sporidesmin hepatotoxicity - Facial Eczema
34
What is Phmopsin a product of
Fungus Diaporthe toxica - grows on lupin stubble
35
What animals does Phmopsin and what does it cause
* Sheep, cattle, occ. horses * Subacute chronic toxicity * Jaundice, secondary photosensitisation
36
Pathology of Phmopsin
Liver shrunken and fibrotic
37
Histopathology of Phmopsin
* Scattered hepatocyte necrosis * Abronmal nitotic figures * Diffuse fibrosis and biliary hyperplasia
38
Lupins infected with fungus Diaporthe toxica -\> acute or chornic signs of liver failure
39
What is seen with blue-green alage acute intoxication
* Diarrhoea, prostration, death * Can cause signs of liver failure if survive
40
Patholog changes with blue green algae
* Haemorrhagic gatro-enteritis * Swollenhaemorrhagic liver
41
What does white phosphorus cause
* Directly toxic * Jaundice * Fattyliver * Periportal fibrosis
42
What does carbon tetrachloride need and casue
1. Activation to free radical CCl3- \> causes lipid peroxidation of membranes 2. Centrolobular necrosis
43
What does Xylitol cause
* Hyperinsulinaemia, hypoglycaemia, icterus * Vomiting, lethargy and weakness * Centrilobular to massive hepatocellular necrosis and periportal vacuolar change
44
What does the ingestion of copper cause
1. Chronic hepatic intoxication and injury 2. Acute haemolytic anaemia in ruminants
45
What does the ingestion of iron cause
* Iron dextran intoxication in piglets * Ferrous fumarate intoxication in foals
46
What drugs are cats susceptible to
* Para-acetylaminophenol: deficient in glucaronyl transferase * Diazepam
47
What drugs are dogs suceptible to
* Carprofen * Long term anticonvulsants

Pathology (26 decks)

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