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POD from G > 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
what form of iron is more readily absorbed
ferrous (2+) more than ferric (3+)
26
T/F heme iron is absorbed more readily than ferric iron
T
27
Iron has negative interactions with what 3 minerals
Cu, P, Zn
28
iron is distributed bound to ___________ and deposited in tissues as (2)
transferrin ; hemosiderin, ferritin
29
how is iron excreted
in sloughed intestinal epithelium; it is limited
30
what is the MOA of iron toxicity
oxidative stress -> lesions in liver and GI tract
31
what type of iron causes oxidative stress
free iron (i.e there is too much iron for the transport capacity of transferrin)
32
where does iron toxicity cause lesions (4); what is most common
liver, heart, pancreas, GI tract liver most common
33
how many stages of iron toxicity are there
4
34
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):
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
how do we diagnose iron toxicity
- 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
how do we treat iron toxicity (4)
remove source, decontaminate, limit further absorption with milk of magnesia, chelate with deferoxamine mesylate
37
astragalus accumulates what metal
selenium
38
what are the signs of zinc toxicity
GI upset, renal failure, hemolysis, hemoglobinuria
39
what is caused by the following cases of selenium toxicity: acute: chronic:
acute: cardiovascular injury chronic: lesions in hooves/skin/hair; weight loss; posterior paralysis; impaired immune system; reproductive effects
40
how do we diagnose selenium toxicity
history, clinical signs, quantification in serum/whole blood/tissue (liver), environment
41
what are the 2 chemical forms of mercury
inorganic (elemental, salts); organic (methylmercury)
42
what type of mercury is readily absorbed orally
methylmercury (organic mercury)
43
what are some sources of mercury
environment, paints, thermometers, fungicides, batteries
44
what are the 2 medicinal uses of mercury
amalgams for dentistry; antiseptics
45
T/F mercury bioaccumulates
T
46
what are the main MOA of mercury
crosses BBB causing neuronal degeneration, reduces protein synthesis, causes lipid peroxidation
47
what are the main clinical signs of mercury toxicosis (5)
GI irritation: nausea, vomiting, diarrhea Cardiac: hypertension, tachycardia CNS injury acute and chronic kidney injury reproductive problems
48
how do we diagnose mercury toxicosis
history, clinical signs, blood hb, heavy metals in tissue, non-specific lesions
49
give an example of the following forms of arsenic: - inorganic - organic
inorganic: naturally occurs in groundwater organic: shellfish
50
what are some sources of arsenic
CCA treated lumber, herbicides, fungicides, groundwater, shellfish
51
is trivalent or pentavalent arsenic more toxic
trivalent
52
how is arsenic absorbed
orally or via skin
53
how is arsenic eliminated
urine, bile, feces, sweat
54
where does arsenic accumulate
liver
55
chronic exposure to arsenic results in accumulation where (3)
hair, nails, feathers
56
what is the MOA of arsenic
trivalent (arsenite) interferes with Krebs; pentavalent (arsenate) uncouples oxidative phosphorylation (no ATP production)
57
arsenic toxicosis impacts what body systems (4)
GI tract, cardiovascular, renal, CNS
58
how do we diagnose arsenic poisoning
levels in liver, kidney, feces, vomit, urine; organic arsenic in brain; exposure in hair and epidermis
59
what are 2 key toxic compounds in smoke and what do they do
carbon monoxide and cyanide -> cellular asphyxiation
60
what are the respiratory effects of the following: - formaldehyde - glutaraldehyde
formaldehyde: loss of cilia, necrosis, inflammation glutaraldehyde: squamous metaplasia
61
carbon monoxide is the product of __________________ of ____________________
incomplete combustion; carbon containing fuels
62
what are some sources of carbon monoxide
internal combustion engines, fireplaces, gas or kerosene heaters, defective furnaces
63
blister beetles contain ___________, which causes
canthardin; vesicles and necrosis in the GI tract
64
biotoxins from spiders cause (3)
pain, muscle cramps, paralysis
65
biotoxins from caterpillars cause
placentitis and abortion in mares
66
venom from rattlesnakes contains (3), which causes (9)
phospholipases, myotoxic peptides, other toxins causes: - pain - local necrosis and hemorrhage - hemolysis and hemoglobinuria - coagulopathy - rhabdomyolysis - myoglobinuria - shock - circulatory collapse
67
what do polychlorinated biphenyls (PCBs) do (2)
endocrine disruptors; carcinogens (some)
68
T/F polychlorinated biphenyls bioaccumulate and persist in the environment
T

POD from G (46 decks)

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