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Pathology > Lecture 18 > Flashcards

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
Q

Where is chornic toxicity with cycads and zamia plams seen and what is the effect

A

Cattle

  • Hepatic necrosis and dissecting fibrosis
26
Q

What produces aflatoxin

A

Product of fungus: Aspergillis flavus, A. parasiticus, Penicillium puberulum

27
Q

Where is acute aflatoxosis usually seen and what does it cause

A

Dogs

Haemorrhagic centrolobular to massive necrosis

28
Q

What is seen with chronic alflatoxicosis

A
  • Shrunken fibrotic liver
  • Fatty change, biliary hyperplasia, centrilobular fibrosis, metalocytosis
29
Q
A

Chronic hepatic aflatoxicosis: fatty change and biliary hyperplasia

30
Q

What is sporidesmin and its cause

A

Facial eczema​

  • Product of fungus Pithomyces chartarum
    • Grows in moistened dead rye grass
    • Cause cholestasis and failure to ecvrete phylloerythrin
31
Q

What is the gross pathology of Sporidesmin

A
  • Secondary photosensitisation esp on face
  • Bile stained liver
32
Q

What is the histopathology fo sporidesmin

A
  • Cholangitis and cholestasis
  • Necrosis of biliary epithelium
  • Dilatele ducts
33
Q
A

Sporidesmin hepatotoxicity

  • Facial Eczema
34
Q

What is Phmopsin a product of

A

Fungus Diaporthe toxica - grows on lupin stubble

35
Q

What animals does Phmopsin and what does it cause

A
  • Sheep, cattle, occ. horses
  • Subacute chronic toxicity
  • Jaundice, secondary photosensitisation
36
Q

Pathology of Phmopsin

A

Liver shrunken and fibrotic

37
Q

Histopathology of Phmopsin

A
  • Scattered hepatocyte necrosis
  • Abronmal nitotic figures
  • Diffuse fibrosis and biliary hyperplasia
38
Q
A

Lupins infected with fungus Diaporthe toxica -> acute or chornic signs of liver failure

39
Q

What is seen with blue-green alage acute intoxication

A
  • Diarrhoea, prostration, death
  • Can cause signs of liver failure if survive
40
Q

Patholog changes with blue green algae

A
  • Haemorrhagic gatro-enteritis
  • Swollenhaemorrhagic liver
41
Q

What does white phosphorus cause

A
  • Directly toxic
  • Jaundice
  • Fattyliver
  • Periportal fibrosis
42
Q

What does carbon tetrachloride need and casue

A
  1. Activation to free radical CCl3- > causes lipid peroxidation of membranes
  2. Centrolobular necrosis
43
Q

What does Xylitol cause

A
  • Hyperinsulinaemia, hypoglycaemia, icterus
  • Vomiting, lethargy and weakness
  • Centrilobular to massive hepatocellular necrosis and periportal vacuolar change
44
Q

What does the ingestion of copper cause

A
  1. Chronic hepatic intoxication and injury
  2. Acute haemolytic anaemia in ruminants
45
Q

What does the ingestion of iron cause

A
  • Iron dextran intoxication in piglets
  • Ferrous fumarate intoxication in foals
46
Q

What drugs are cats susceptible to

A
  • Para-acetylaminophenol: deficient in glucaronyl transferase
  • Diazepam
47
Q

What drugs are dogs suceptible to

A
  • Carprofen
  • Long term anticonvulsants

Pathology (26 decks)

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