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Toxicology > Unit 1 - Heavy Metals > Flashcards

Unit 1 - Heavy Metals Flashcards

1
Q

What is one of the top bovine poisonings that we see in the diagnostic lab?

A

lead

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2
Q

What are the most common sources of small animal lead toxicosis?

A

Paint chips/dust, fishing tackle, lead based toys, and lead shot/bullets

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3
Q

What species is most often affected by lead based paint?

A

goats and poultry

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4
Q

What species is most often affected by lead shot?

A

water fowl

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5
Q

What species are most often affected by lead based toys and fishing tackle?

A

Dogs

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6
Q

What are the most common sources of large animal lead toxicosis?

A

Lead batteries, motor oil, old building foundations, old pesticides, and paint

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7
Q

(Cows/calves) get seasonal lead toxicosis in the (spring and summer/fall and winter).

A

Calves, spring/summer

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8
Q

What age group and season do dogs typically get lead toxicosis?

A

Dogs are indiscriminate eaters so they can get it at any age and in any season

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9
Q

What birds typically get lead poisoning?

A

Chickens, water fowl, and raptors

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10
Q

If calves on pasture aren’t dying from ______ or _____, then lead should be next on the list.

A

GI or respiratory illnesses

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11
Q

What are the human health implications with lead toxicosis in chickens?

A

Egg contamination

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12
Q

Overall, what age group is more susceptible to lead toxicosis?

A

younger animals

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13
Q

What type of environment leads to increased absorption of lead?

A

acidic environment

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14
Q

Lead is absorbed in the _________, enters the _______, is deposited in _________, crosses the ______, and is excreted in ____ and ______.

A

GI tract, bloodstream, bone, BBB, feces and milk

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15
Q

What are the MOAs of lead?

A
  1. Binds to sulfhydryl groups which decreases heme synthesis
  2. Displaces Ca from binding sites which alters nerve and muscle transmission
  3. It inhibits membrane enzymes which decreases smooth muscle contraction
  4. It interferes with mineral absorption (Ca and calbindin)
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16
Q

When does the onset of clinical signs occur in cases of lead toxicosis?

A

48 hours

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17
Q

What clinical signs predominate in dogs with lead toxicosis?

A

GI signs - vomiting, anorexia, diarrhea, and a tender abdomen

These are the first signs to occur

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18
Q

What clinical signs occur 2nd in lead toxicosis in dogs?

A

Neurologic signs - lethargy, ataxia and blindness, hysteria and convulations/seizures, and mydriasis

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19
Q

What clinical signs predominate in cattle with lead toxicosis?

A

Neurologic signs - blindness, increased vocalization, ataxia, head pressing, tremoring and convulsions, bruxism, circling, and aimless wandering

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20
Q

What clinical signs may or may not happen in lead toxicosis cattle?

A

GI signs - anorexia. rumen stasis, and gaunt

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21
Q

T/F - Lead should always be on your list for neurologic cattle

A

True

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22
Q

What clinical signs are associated with lead toxicosis in cats?

A

Non-specific - lethargy, anorexia, vomiting, and weight loss

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23
Q

What clinical signs are associated with lead toxicosis in birds?

A

Neurologic signs - Depression, ataxia, weight loss, esophageal paralysis, regurgitation, wing droop

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24
Q

What clinical signs are associated with lead toxicosis in horses?

A

Neurologic - paralysis of recurrent laryngeal nerve and ataxia

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25
What samples should be taken for detection of lead in lead toxicosis cases?
Whole blood and milk Liver, kidney, bone, and GI contents Unknowns and feed
26
Aside from testing for lead, what else would you use a whole blood sample for in a case of lead toxicosis?
Blood smear
27
What would a brain sample be used for in cases of lead toxicosis?
Histopathology
28
What will you see on a blood smear in a dog with lead toxicosis?
Nucleated RBCs, basophilic stippling, and NO anemia
29
What other diagnostic tool could be helpful if you suspect lead toxicosis?
Radiographs
30
What gross lesions does lead toxicosis cause?
Fluorescence of laminal cortical region in the brain | emaciated muscle wasting in birds
31
What microscopic lesions does lead toxicosis cause?
laminar cortical necrosis | Dogs - acidophilic intra-nuclear inclusion bodies
32
What else causes the 'polio' lesion that lead toxicosis causes?
Thiaminases Water deprivation Thiamine deficiency Sulfur intoxication
33
How is lead toxicosis treated?
Eliminate the exposure - remove the source or the animal | Stop further absorption
34
How do you stop further absorption of lead?
Decontaminate the GI tract and remove the Pb object
35
What chelator is the best treatment for lead toxicosis that does not increase Pb absorption?
Succimer (DMSA)
36
What chelator may increase Pb absorption if the object is still in the patient when treating for lead toxicosis?
CaEDTA (most common in cattle)
37
What other chelator can be used to treat lead toxicosis?
D-penicillamine and Dimercaprol (BAL)
38
T/F - There is one legal FDA approved antidote for lead toxicosis in LA.
False - there are none
39
What environmental and human health impacts does lead have?
There is a public health concern and food safety concern (secreted in milk and residue in bone)
40
What happens if lead toxicosis is affected at a herd level?
Contact a state veterinarian
41
What are the different forms of arsenic and which is the most toxic?
Trivalent (3+), Pentavalent (5+) and organic Trivalent is 10x more toxic
42
T/F - Like lead, arsenic is considered a carcinogen.
True
43
What are the sources of arsenic?
Insecticides, herbicides, wood preservatives, swine and poultry feed additives, mining sites and smelters, and old heartworm treatment
44
Arsenic has _____ absorption, accumulates in the ______, and is rapidly excreted in the ______.
variable, liver, feces
45
What does arsenic toxicity depend on?
Solubility, route of administration, absorption, and metabolism
46
What does the kidney do to pentavalent arsenic?
It converts to trivalent arsenic
47
If you find arsenic in the skin or the hair, what does that indicate?
It was chronic toxicity
48
What is the MOA of trivalent arsenic?
It binds to sulfhydryl compounds and blocks cellular respiration
49
How does trivalent arsenic cause edema?
It causes capillary dilation
50
What is the MOA of pentavalent arsenic?
It substitutes for P and uncouples oxidative phosphorylation
51
What are the main clinical signs associated with arsenic toxicosis?
GI - vomiting, colic/intense abdominal pain, diarrhea, weakness and ataxia, and acute death
52
Aside from GI signs, what other signs does arsenic cause?
renal - oliguria
53
What clinical signs do swine exhibit with arsenic toxicosis?
Reduce motor control, goose-stepping, blindness, non-ambulatory (non-painful), and incoordination and lack of proprioception
54
What samples should be sent to histopath for arsenic diagnosis?
Sciatic nerve, optic nerve, kidney, liver, and GI tract
55
What tissues should be collected for heavy metal/As analysis?
Liver, kidney, brain, hair, urine, feed, and unknown
56
What gross lesions are associated with arsenic toxicosis?
Necrohemorrhagic gastroenteritis, edema, ulcerations, pale kidneys, and pale yellow liver
57
What microscopic lesions are associated with arsenic toxicosis?
GI and renal necrosis, submucosal edema, peripheral neuromuscular degeneration, edema of white matter, degenerative neurons, and degeneration of the optic nerve
58
What are the different forms of mercury in order of toxicosis?
Organic > inorganic > Elemental
59
What are the elemental sources of mercury?
Thermometers, barometers, and fluorescent tubes
60
What are the inorganic sources of mercury?
Salts and button batteries
61
What are the organic sources of mercury?
Marine fish/shellfish | Fungicides
62
What are the main marine fish that are sources of organic mercury and why?
Sharks, mackerel, and swordfish | They are at the top of the food chain
63
The ______ form of mercury is slowly absorbed orally, and rapidly absorbed via inhalation.
Elemental
64
The _______ form of mercury has slow absorption, accumulates in the kidney, and is excreted in the urine.
Inorganic
65
The organic form of mercury is lipophilic so it is ______ absorbed. It accumulates in the ______, and is excreted in _______.
Readily, brain, feces
66
T/F - All forms of mercury can cross the placenta and accumulate in the fetus.
True
67
What is the MOA of mercury?
Just know that it results in necrosis
68
When does the onset of clinical signs for inorganic mercury toxicosis occur?
Within hours
69
What are the clinical signs of inorganic mercury toxicosis?
GI irritation and inflammation, vomiting, diarrhea, stomatitis Oliguria Death
70
When does the onset of clinical signs for organic mercury toxicosis occur?
7-10 days
71
What are the early clinical signs of organic mercury toxicosis?
Irritation of the dermis and mucous membranes, conjunctivitis, lacrimation, and stomatitis
72
What are the intermediate clinical signs of organic mercury toxicosis?
Neurologic - blindness, ataxia, and paresis
73
What are the advanced clinical signs of organic mercury toxicosis?
Abnormal posture, blindness, anorexia, paralysis coma, and death
74
T/F - The mortality rate for mercury toxicosis is low.
F - it is high
75
What samples are important to get to diagnose acute mercury toxicosis?
whole blood and urine
76
What samples are the best for detecting mercury?
Liver, kidney, and brain
77
What GI lesions are associated with mercury toxicosis?
ulcerative and necrotic gastroenteritis
78
What renal lesions are associated with mercury toxicosis?
Pale/swollen kidneys and tubular necrosis
79
What neurologic lesions are associated with mercury toxicosis?
Swine - demyelination of peripheral nerves | Cats - cerebellar hypoplasia
80
How is elemental/inorganic mercury toxicosis treated?
Oral decontamination - egg whites, saline cathartic or sorbitol, Na thiosulfate, D-penicillamine
81
Why is organic mercury toxicosis often not treated?
Because the damage is too extensive and it is too late
82
What environmental and human health considerations are there for mercury toxicosis?
There is bioaccumulation and biomagnification

Toxicology (32 decks)

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