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Toxicology > Lecture 18 - Hematoxicology 2 > Flashcards

Lecture 18 - Hematoxicology 2 Flashcards

1
Q
  1. What plant is pictured below?
  2. Where can this plant be found?
A

Red Maple (Acer rubrum)
 Found in the entire eastern US
and Canada

Red maple (Acer rubrum) is a deciduous tree native to eastern North America
but is found as far west as Texas.
Red maple is planted as an ornamental because of its vibrant fall colours, and
it thrives better in altered environments and has outcompeted rival species.

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2
Q

Red Maple (Acer rubrum)
Toxic principles: ___________
○ ______ acid and ______

A

oxidants, Gallic, tannins

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3
Q

Red Maple (Acer rubrum)
Species affected?

A

: equine (horses, ponies, Grevy’s zebra) following ingestion of wilted or dried leaves. Bark also is toxic

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4
Q

Red Maple (Acer rubrum) ADME
 _______ acid is metabolized to ________ acid in equine ileum by ___________ ______ or ____________________-
 _______ acid is further metabolized to ________ in equine ileum also by ___________ ______ or ____________________
 ___________ is absorbed in equine ileum and
interacts with ____ (Fe) to form _____ ________
leading to the oxidation of ____ to ____ in Hb to form ________

A

 Tannic acid is metabolized to gallic acid in equine
ileum by Klebsiella pneumoniae or Enterobacter
cloacae
 Gallic acid is further metabolized to pyrogallol in
equine ileum also by K. pneumoniae or E.
cloacae
 Pyrogallol is absorbed in equine ileum and
interacts with iron (Fe) to form free radicals
leading to the oxidation of Fe2+ to Fe3+ in Hb to
form methemoglobin

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5
Q
A
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6
Q

What is the MOT of Red Maple Toxicosis?

 Oxidative damage of Hb → precipitation of
oxidized Hb as ______ _____ in the RBCs →
RBCs are then removed by the ______
(extravascular hemolysis)
 Damage to RBC membranes → altered
_________ → intravascular ________
 Both processes result in severe progressive
_______
 In addition, hemoglobin is filtered in _____ →
________ in renal tubules → renal ________

A

Mechanisms of Toxicity
 Oxidative damage of Hb → precipitation of
oxidized Hb as Heinz bodies in the RBCs →
RBCs are then removed by the spleen
(extravascular hemolysis)
 Damage to RBC membranes → altered
permeability → intravascular hemolysis
 Both processes result in severe progressive
anemia
 In addition, hemoglobin is filtered in kidney →
precipitation in renal tubules → renal failure

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7
Q

What are the clinical signs of red maple toxicosis?

A

 Poisoning is more likely in fall/late summer or
after a storm when fallen red maple leaves/tree
branches are accessible to horses. Poisoned
animals display:
 Depression, anorexia, acute hemolytic anemia
with weakness, increased respiratory and heart
rates, cyanosis, icterus, and a red-brown
coloration of the urine, decreased PCV, Heinz
bodies, proteinuria, weakness, coma and death
 Abortion may occur in pregnant mares
 Paracute death from tissue anoxia may occur

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8
Q

How do you Dx Red Maple Toxicosis?

 History of ________ to red maple leaves
 Poisoning occurs primarily between ____ and _____
 ________ signs
 Rule out other causes of _______ ______

A

 History of exposure to red maple leaves
 Poisoning occurs primarily between July and October
 Clinical signs
 Rule out other causes of hemolytic anemia

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9
Q

What are your DDx for Red Maple Toxicosis?

A

Causes of hemolytic anemia
 Equine infectious anemia
 Piroplasmosis
 Ehrlichiosis
 Onion toxicosis
 Nitrate/nitrite toxicosis
 Brassica toxicosis
 Naphthalene toxicosis

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10
Q

How do you Tx Red Maple Toxicosis?

A
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11
Q

Allium (?)
 Herbaceous plants with bulbs
 Domesticated and wild varieties
 Found throughout North America
 Toxic principle: ?

A

Allium (Onion, Garlic, Leek, Chives)
 Herbaceous plants with bulbs
 Domesticated and wild varieties
 Found throughout North America
 Toxic principle: n-propyl disulfide and other disulfides

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12
Q

List the exposure and risk factors for allium toxicity?

A
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13
Q

What is the toxic dose of allium toxicosis?

A
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14
Q

What is the MOT of Allium toxicosis?

Affects the enzyme ______-__-_______________ _________ thereby impairing the hexose monophosphate pathway in RBCs
 Oxidation of Hgb results due to insufficient
________ or _________
 The oxidized Hgb precipitates in the RBCs to
form _______ ________
 RBCs with _______ _______ are removed in the spleen or undergo hemolysis → ________
 ______ are highly sensitive because their Hb is
more sensitive to oxidative damage

A

Affects the enzyme glucose-6-phosphate dehydrogenase thereby impairing the hexose monophosphate pathway in RBCs
 Oxidation of Hgb results due to insufficient
NADPH or glutathione
 The oxidized Hgb precipitates in the RBCs to
form Heinz bodies
 RBCs with Heinz bodies are removed in the
spleen or undergo hemolysis → anaemia
 Cats are highly sensitive because their Hb is
more sensitive to oxidative damage

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15
Q
A
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16
Q

What are the clinical signs of allium toxicosis?

A

 Anorexia, vomiting, salivation, lethargy, ataxia or
recumbency, rapid breathing and heart rates,
pale or icteric mucous membranes, onion odor
in breath and onion flavor in milk
 Pregnant animals may abort
 Hemoglobinemia, hemoglobinuria (dark red-
brown urine), reduced PCV and hematocrit,
Heinz bodies may be seen in RBCs, elevated
WBC count

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17
Q
A
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18
Q

How do you Dx Allium toxicosis?

A

Dx
 Hematological parameters and urine appearance
 History, clinical signs and examination of pasture
or property for Allium spp.

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19
Q

How do you treat Allium toxicosis?

A

Tx
 Decontaminate: emesis (within 1 h), gastric
lavage (within 2-4 h), activated charcoal plus
cathartic (e.g., sorbitol)
 Maintain cardiovascular support
 IV fluids
 Oxygen
 Whole blood transfusion or Oxyglobin

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20
Q
A

Bracken Fern (
Pteridium aquilinum)
 Native perennial herb
 Occurs throughout the US
 Young plants and rhizomes
are the most toxic
 Toxic principles:
 Thiaminase
 Ptaquiloside
 Cyanogenic glycoside

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21
Q

What is the Mechanisms of Toxicity of
Ptaquiloside

 Causes death of __________ cells in bone marrow
 Causes urinary tract _______
 Ptaquiloside causes DNA _______ and induction of _________
 Ptaquiloside is secreted in ____ (the milk causes
__________ in mice)

A

 Causes death of precursor cells in bone marrow
 Causes urinary tract neoplasia
 Ptaquiloside causes DNA alkylation and induction of
protooncogenes
 Ptaquiloside is secreted in milk (the milk causes
neoplasia in mice)

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22
Q

Disease Syndromes Caused by Bracken Fern

A
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23
Q

Clinical signs of bracken fern toxicosis?

A

 Suppression of bone marrow activity occurs
after >3-4 weeks of exposure
 There is severe pancytopenia with acute
onset of fever, lethargy and loss of appetite
 Hemorrhaging via natural orifices: vulva,
mouth, conjunctiva and anterior chamber of
the eye
 Bloody stool and urine

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24
Q

What can happen as a result of prolonged consumption of bracken fern?

A

Enzootic Hematuria
Red Water disease
 Intermittent blood loss in urine from
hemorrhages and tumors in the urinary
bladder
 Occurs after prolonged (2 years) consumption
of low levels (<10g/kg/d) bracken fern
 Results in anemia, elevated heart rate,
weakness
○ Death from anemia

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25
GI tract tumors result in:
 Choking, coughing, bloat, emaciation  Regurgitation of greenish fluid and extended neck posture
26
How do you Dx Bracken Fern toxicosis?
 History of exposure to bracken fern over several weeks to months  Compatible clinical signs and lesions
27
How do you Tx Bracken Fern toxicosis?
 Blood or platelet transfusion in cattle for aplastic anemia  Antibiotics to prevent secondary infections
28
List the sources of Brassica.
Sources: Cabbage, kale, broccoli, turnips, mustards, etc. Often used as winter feed for cattle and sheep
29
What are the toxic principles of Brassica?
 Toxic principles  S-methyl cysteine sulfoxide (SMCO)  Others: glucosinolates, goitrin, nitrile and nitrates
30
What species are susceptible to brassica toxicosis?
poultry, swine, cattle, sheep
31
Brassica toxicosis - ADME  SMCO is reduced to toxic dimethyl disulfide by microbial fermentation in the GI tract  Absorption and metabolism take <1 day
32
What is the MOT of brassica toxicosis?
Dimethyl disulfide is an oxidant  Oxidizes hemoglobin to form Heinz bodies → hemolytic anemia Glucosinolates give rise to isothiocyanates which cause gastroenteritis  Goitrin is goitregenic  Nitrate is converted to nitrite in rumen → oxidation of Hgb → methemoglobinuria  Nitrile causes pulmonary emphysema, hepatic necrosis and blindness
33
What are the clinical signs of brassica toxicosis?
 Anemia and GI upset are the most common signs  Hemoglobinuria(emia), tachycardia, polypnea, cyanosis and jaundice may be observed  Scouring, colic, rumen stasis  Poor conception rate, reduced milk production and growth retardation  Goiter
34
How do you Dx Brassica toxicosis?
 Presence of Brassica, evidence of consumption and appropriate clinical signs
35
How do you treat brassica toxicosis?
Mostly supportive  Blood transfusion  Diuresis with fluids to reduce occurrence of hemoglobinuric nephrosis
36
What species are susceptible to Cu toxicosis?
all
37
List the different Cu toxicities.
 Acute copper toxicosis in sheep  Enzootic icterus in sheep (South Africa)  Genetic canine copper toxicosis in Bedlington terriers, West Highland white terriers, Skye terriers, Dalmatian, Doberman pinschers ○ In Bedlington terriers it is due to an autosomal recessive disorder of biliary Cu excretion Wilson’s disease in humans
38
What are the causes of acute copper toxicosis?
--> Causes: ingestion or administration of Cu- containing formulations or material:  Anthelmintics, footbaths, pesticides, dietary additives, copper salts, environmental contamination, poultry litter, coins  Feeding of calf, horse, poultry or swine food to sheep
39
What are the risk factors of acute copper toxicosis?
Feeding ionophores (e.g., monensin) increase Cu absorption and toxicity
40
Which species are sensitive to acute copper toxicosis?
41
What is the MOT of acute copper toxicosis?
Necrotic hepatocytes release Cu to blood circulation → Cu damages RBCs → intravascular hemolysis and release of Hgb  Lysis of RBC causes anoxia → centrilobular hepatic necrosis and more release of Cu, which accumulates in other tissues such as the kidney
42
What is the MOT of acute copper toxicosis? _________ hepatocytes release Cu to blood circulation → Cu damages _____ → intravascular _______ and release of ____ --> Lysis of RBC causes _____ → ________ hepatic necrosis and more release of Cu, which accumulates in other tissues such as the kidney
Necrotic hepatocytes release Cu to blood circulation → Cu damages RBCs → intravascular hemolysis and release of Hgb  Lysis of RBC causes anoxia → centrilobular hepatic necrosis and more release of Cu, which accumulates in other tissues such as the kidney
43
What is the MOT of acute copper toxicosis?
Necrotic hepatocytes release Cu to blood circulation → Cu damages RBCs → intravascular hemolysis and release of Hgb  Lysis of RBC causes anoxia → centrilobular hepatic necrosis and more release of Cu, which accumulates in other tissues such as the kidney --> Inactivation of proteins  Displacement of other essential metals e.g. Zn from their proteins  Oxidation of –SH groups and depletion of antioxidants (e.g., GSH) → oxidative stress → oxidation of biomolecules (membrane lipid, proteins and DNA)
44
What are the clinical signs of acute copper toxicosis in sheep?
Sheep (and cattle)  Rarely show signs until stressed → massive liver necrosis → Cu release → RBC damage → hemolysis → hemoglobinuria, icterus, anoxia and death  Hemolytic crisis: dark-red (port wine) urine, swollen gunmetal-blue kidneys, swollen spleen with dark brown-black parenchyma stress: ↓Food intake * Transportation * Handling, shearing * Extreme weather * Exercise
45
What are the clinical signs of acute copper toxicosis in swine?
generally resistant  Young swine are more susceptible than adults  Anorexia, depression, poor weight gain, icterus, hemoglobinuria and bloody feces are observed
46
47
- Acute Cu toxicity is rare in cats and dogs - Commonly associated with ingestion of pennies  Canadian pennies minted up to 1997 contain 98.5% Cu  Some US pennies minted up to 1983 contain 95% Cu  Note: Canadian penny was discontinued in 2013 - Typical signs include depression, dehydration, anorexia, intermittent vomiting, mild abdominal pain and diarrhea
48
Describe copper storage disease in dogs
49
Subacute Cu Poisoning  Occurs in lambs in Cu-deficient areas like FL, other south-eastern coastal areas, and west of Rockies  Toxicosis results from administration of Cu compounds (even at normal dosage!)  Signs include GI tract hemorrhage, pulmonary edema and ascites. There is liver damage but no icterus or hemolytic crisis
50
How do you Dx subacute cu poisoning?
 History  Evidence of blue-green ingesta  Elevated serum & liver/kidney Cu concentrations  CBC and serum panel  Check for evidence of hemolysis, elevated liver enzymes and other indicators of liver dysfunction  Abdominal radiographs: foreign objects e.g., coins  Liver histopathology  Breed of dog
51
How do you Tx subacute cu poisoning in small animals?
 Surgery to remove foreign body  Supportive care, e.g., IV fluids  D-penicillamine to chelate Cu and promote its urinary excretion
52
How do you Tx subacute cu poisoning in ruminants?
 Treatment of acute Cu toxicosis often not successful  Ammonium molybdate, sodium thiosulfate or ammonium tetrathiomolybdate to reduce liver [Cu]  Dietary supplementation with zinc acetate to reduce Cu absorption
53
List the sources of Zinc
Consumption of zinc sources or zinc- containing foreign bodies  Pennies: US pennies after 1982: 97.5% Zn. Canadian pennies 1997-2001: 96% Zn  Galvanized metal, pennies, diaper rash ointment, zinc oxide sunscreen, feed mixing error, forage close to industries etc
54
Which species are at risk of Zinc toxicosis?
all, dogs (small breeds, younger dogs) mainly, caged birds
55
Zn is an ?
Essential trace mineral
56
Zinc ADME  Small intestine is the main site of absorption  Absorption is affected by several factors:  Dietary components (Cu2+, Ca2+, Mg2+, phytate, protein), age, growth rate  Excretion  In bile via feces, intestinal mucosal secretions and pancreatic fluid. Some chelated Zn is lost via urine
57
What is the MOT of Zinc toxicosis?
1. Direct irritation of GI tract → GI signs 2. Zinc causes hemolytic anemia due to:  Direct damage to RBC membranes  Inhibition of RBC enzymes  Increased RBC susceptibility to oxidative damage 3. Competitive interactions with Cu & Fe (causes enemia) and Ca
58
What are the clinical signs of Zinc toxicosis?
Depression, vomiting, diarrhea, anorexia, abdominal pain  ^ number of nucleated RBCs, ^basophilic stippling (aggregation of ribosomal RNA in RBCs)  Icterus, hemolytic anemia, decreased PCV, hemoglobinemia, hematuria, weakness and death  Cu deficiency may occur in sheep
59
How do you Dx Zinc toxicosis?
Zinc analysis in serum, kidney, liver and urine  Collect serum in royal blue-top tubes (have plastic stoppers). Syringes used to collect blood should not have rubber (rubber is contaminated with Zn)  Radiography  DDx: Onion, copper, mothballs, nitrate/nitrite, and acetaminophen toxicoses, propylene glycol toxicosis, naphthalene toxicosis
60
61
How do you Tx Zinc Toxicosis?
1. Symptomatic and supportive  IV fluids, electrolytes, blood transfusion  Diuresis with a balanced crystalloid solution 2. Remove zinc foreign body: endoscopic or surgical (gastrotomy or enterotomy) 3. Proton pump inhibitors, H2-blockers and sucralfate 4. Chelation therapy: Ca-EDTA, BAL or D- penicillamine
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Toxicology (32 decks)

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