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POD > 4.4 Metals and Environmental Toxicants > Flashcards

4.4 Metals and Environmental Toxicants Flashcards

1
Q

hard metals follow what kind of curve

A

dose-response (i.e. too deficient or too much leads to toxicity)

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2
Q

give an example for the following functions of metals in the body:
- cofactors for many enzymes, ex. kinases
- oxygen transport
- antioxidants
- bone formation
- endocrine
- muscle contraction
- immune function

A
  • cofactors for many enzymes, ex. kinases -> Mg
  • oxygen transport -> heme Fe
  • antioxidants -> Se containing glutathione
  • bone formation -> Ca, P
  • endocrine -> iodine for thyroid hormone
  • muscle contraction -> Ca
  • immune function -> Zn
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3
Q

what are some sources of lead

A

old paint, leaded gasoline, plumbing pipes, ammunition, fish sinkers, construction materials, stained glass, toys

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4
Q

what are the 3 forms of lead and some examples

A

1) metallic aka elemental lead: batteries, weight to balance tires
2) inorganic lead: old paints
3) organic lead: gasoline additives

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5
Q

what is the difference between elemental, inorganic and organic lead

A

elemental/metallic: pure Pb
inorganic: bound to other elements
organic: bound to carbonated groups (methyl, ethyl)

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6
Q

what are the signs of ACUTE lead toxicosis

A

gastropathy, lethargy, anorexia, anemia, encephalopathy, neuropathy

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7
Q

what are the signs of CHRONIC lead toxicosis

A

weight loss, impaired bone growth, peripheral neuropathy, impaired brain development in children

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8
Q

lead toxicosis MOA involves conversion of ___________ to ___________

A

δ-aminolevulinic acid -> protoporphyrin

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9
Q

what does lead do to RBCs

A

inhibits maturation by binding to RBCs -> rubricytosis and basophilic stippling observed on blood smear

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10
Q

rubricytosis in the absence of a regenerative response is indicative of what toxicity

A

lead

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11
Q

acute lead toxicity is associated with what neurologic condition

A

polioencephalomalacia

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12
Q

lead poisoning in waterfowl and raptors is associated with what? what are the clinical signs

A

peripheral neuropathy:
- demyelination of Schwann cells
- peripheral motor nerve dysfunction

muscle wasting, muscle weakness, inability to feed

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13
Q

how do we diagnose lead toxicity (4)

A
  • history of exposure
  • clinical signs
  • x-rays
  • hematology (rubricytosis, basophilic stippling, anemia)
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14
Q

lead is 90% bound to

A

RBCs

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15
Q

what species absorbs copper from the diet very efficiently but excrete it slowly

A

sheep

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16
Q

where does copper accumulate/store (3)

A

liver, kidney, brain

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17
Q

T/F copper binds to blood proteins

A

T

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18
Q

Cu bioavailability is reduced by interactions with ____ and ____

A

Mo and S

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19
Q

Cu toxicity causes what injuries (4)

A
  • liver injury/inflammation/fibrosis
  • oxidative stress on RBCs -> hemolysis
  • hyperbilirubinemia -> jaundice
  • hyperbilirubinuria -> nephrosis
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20
Q

what metal is released into the blood under stress

A

copper

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21
Q

chronic copper poisoning is an inherited disease in ____________ (species of dog) due to a mutation in the gene _____________ that results in _________________

A

Bedlington terriers; COMMD1; impaired Cu excretion (accumulation) in hepatocytes and resultant hepatitis

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22
Q

how do we treat copper poisoning in sheep? in dogs?

A

sodium molybdate and sodium thiosulfate; D-penicillamine, triethylene tetramine dihydrochloride

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23
Q

Iron is an essential mineral for (3)

A

Hb, Mb, cytochromes

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24
Q

iron toxicity causes chronic ________ injury

A

hepatic injury (necrosis, fibrosis)

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25
Q

what form of iron is more readily absorbed

A

ferrous (2+) more than ferric (3+)

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26
Q

T/F heme iron is absorbed more readily than ferric iron

A

T

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27
Q

Iron has negative interactions with what 3 minerals

A

Cu, P, Zn

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28
Q

iron is distributed bound to ___________ and deposited in tissues as (2)

A

transferrin ; hemosiderin, ferritin

29
Q

how is iron excreted

A

in sloughed intestinal epithelium; it is limited

30
Q

what is the MOA of iron toxicity

A

oxidative stress -> lesions in liver and GI tract

31
Q

what type of iron causes oxidative stress

A

free iron (i.e there is too much iron for the transport capacity of transferrin)

32
Q

where does iron toxicity cause lesions (4); what is most common

A

liver, heart, pancreas, GI tract

liver most common

33
Q

how many stages of iron toxicity are there

A

4

34
Q

describe the signs for the following stages of iron toxicity:

Stage 1 (0-6h):
Stage 2 (6-24h):
Stage 3 (<4 days):
Stage 4: (2-6 weeks):

A

Stage 1 (0-6h): GI (vomiting, diarrhea, bleeding)
Stage 2 (6-24h): latent
Stage 3 (<4 days): lethargy, GI, hypotension, tachycardia, coagulation deficits, hepatic necrosis, +/- death
Stage 4: (2-6 weeks): healing ulcers, fibrosis, strictures

35
Q

how do we diagnose iron toxicity

A
  • history
  • clinical signs
  • elevated liver parameters
  • PM lesions in liver and GI tract
  • serum Fe analysis -> increased total serum Fe, increased TIBC, increased saturation of transferrin
36
Q

how do we treat iron toxicity (4)

A

remove source, decontaminate, limit further absorption with milk of magnesia, chelate with deferoxamine mesylate

37
Q

astragalus accumulates what metal

A

selenium

38
Q

what are the signs of zinc toxicity

A

GI upset, renal failure, hemolysis, hemoglobinuria

39
Q

what is caused by the following cases of selenium toxicity:

acute:
chronic:

A

acute: cardiovascular injury
chronic: lesions in hooves/skin/hair; weight loss; posterior paralysis; impaired immune system; reproductive effects

40
Q

how do we diagnose selenium toxicity

A

history, clinical signs, quantification in serum/whole blood/tissue (liver), environment

41
Q

what are the 2 chemical forms of mercury

A

inorganic (elemental, salts); organic (methylmercury)

42
Q

what type of mercury is readily absorbed orally

A

methylmercury (organic mercury)

43
Q

what are some sources of mercury

A

environment, paints, thermometers, fungicides, batteries

44
Q

what are the 2 medicinal uses of mercury

A

amalgams for dentistry; antiseptics

45
Q

T/F mercury bioaccumulates

A

T

46
Q

what are the main MOA of mercury

A

crosses BBB causing neuronal degeneration, reduces protein synthesis, causes lipid peroxidation

47
Q

what are the main clinical signs of mercury toxicosis (5)

A

GI irritation: nausea, vomiting, diarrhea
Cardiac: hypertension, tachycardia
CNS injury
acute and chronic kidney injury
reproductive problems

48
Q

how do we diagnose mercury toxicosis

A

history, clinical signs, blood hb, heavy metals in tissue, non-specific lesions

49
Q

give an example of the following forms of arsenic:
- inorganic
- organic

A

inorganic: naturally occurs in groundwater
organic: shellfish

50
Q

what are some sources of arsenic

A

CCA treated lumber, herbicides, fungicides, groundwater, shellfish

51
Q

is trivalent or pentavalent arsenic more toxic

A

trivalent

52
Q

how is arsenic absorbed

A

orally or via skin

53
Q

how is arsenic eliminated

A

urine, bile, feces, sweat

54
Q

where does arsenic accumulate

A

liver

55
Q

chronic exposure to arsenic results in accumulation where (3)

A

hair, nails, feathers

56
Q

what is the MOA of arsenic

A

trivalent (arsenite) interferes with Krebs; pentavalent (arsenate) uncouples oxidative phosphorylation (no ATP production)

57
Q

arsenic toxicosis impacts what body systems (4)

A

GI tract, cardiovascular, renal, CNS

58
Q

how do we diagnose arsenic poisoning

A

levels in liver, kidney, feces, vomit, urine; organic arsenic in brain; exposure in hair and epidermis

59
Q

what are 2 key toxic compounds in smoke and what do they do

A

carbon monoxide and cyanide -> cellular asphyxiation

60
Q

what are the respiratory effects of the following:
- formaldehyde
- glutaraldehyde

A

formaldehyde: loss of cilia, necrosis, inflammation

glutaraldehyde: squamous metaplasia

61
Q

carbon monoxide is the product of __________________ of ____________________

A

incomplete combustion; carbon containing fuels

62
Q

what are some sources of carbon monoxide

A

internal combustion engines, fireplaces, gas or kerosene heaters, defective furnaces

63
Q

blister beetles contain ___________, which causes

A

canthardin; vesicles and necrosis in the GI tract

64
Q

biotoxins from spiders cause (3)

A

pain, muscle cramps, paralysis

65
Q

biotoxins from caterpillars cause

A

placentitis and abortion in mares

66
Q

venom from rattlesnakes contains (3), which causes (9)

A

phospholipases, myotoxic peptides, other toxins

causes:
- pain
- local necrosis and hemorrhage
- hemolysis and hemoglobinuria
- coagulopathy
- rhabdomyolysis
- myoglobinuria
- shock
- circulatory collapse

67
Q

what do polychlorinated biphenyls (PCBs) do (2)

A

endocrine disruptors; carcinogens (some)

68
Q

T/F polychlorinated biphenyls bioaccumulate and persist in the environment

A

T

POD (18 decks)

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