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Toxicology Exam 2 > Tox Exam 2 Heavy Metals > Flashcards

Tox Exam 2 Heavy Metals Flashcards

1
Q

Sources of zinc toxicosis?

A

ingestion of excessive zinc from food/beverage stored in galvanized containers, galvanized wire, plumbing nuts, transport cages nuts, batteries, jewelry, trinkets, zinc oxide skin ointment, zinc containing shampoos, lotions and wound healing agents, overdose of dietary zinc supplements, ingestion of US and canadian pennies

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2
Q

What species are susceptible to zinc toxicosis?

A

cattle, sheep, horses, cats, dogs, ferrets, aviary birds

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3
Q

Zinc is a component of these enzymes/proteins?

A

ADH, LDH, ALP, carbonic anhydrase, superoxide dismutase, DNA/RNA polymerase

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4
Q

What does zinc bind to?

A

SH group and phosphate

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5
Q

Zinc is important in these processes in the body?

A

growth, cell proliferation, skeletal development, collagen formation, skin, feathering, wound healing, repro, immune system function, direct stabilizing effect on cellular membranes, for functioning taste and smell receptors

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6
Q

What are the 3 forms of zinc toxicosis?

A

Acute–>LD50–100mg/kg
Subacute–>dogs caused by ingesting 5 pennies
Chronic–>over 2,000 ppm in diet

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7
Q

ADME of zinc?

A

A=20-30% ingested Zn absorbed from GIT by carrier mediated transport
D/M=most rapid accumulation and turnover occurs in pancreas, liver, kidney, spleen and male repro tract
E=feces, bile, saliva, sweat, urine, pancreatic juice, via mucosal cells

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8
Q

T/F An alkaline environment increases Zn release and absorption.

A

FALSE–acidic

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9
Q

What factors decrease GI absorption of Zn?

A

Ca, Cu, Fe, phytate, fibers, alkaline environment

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10
Q

What factors increase GI absorption of Zn?

A

certain AAs, peptides, EDTA, acidic environment

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11
Q

Zinc travels systemically bound to what 2 proteins?

A

albumin–2/3 bound

beta2-macroglobulin–1/3 bound

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12
Q

Clinical signs of Zn toxicosis?

A

GI–>V+, anorexia, lethargy, abdominal pain, D+, pica
hematologic–>hemolytic anemia, icterus, hemoglobinuria
renal–> azotemia, hyperphosphatemia
other–>livestock show decreased wt or milk production, foals show lameness and stiffness

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13
Q

What are the main organs affected by Zn toxicosis?

A

pancreas, liver, kidney, blood (RBCs)

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14
Q

MOA behind hemolytic anemia in Zn toxicosis?

A

possibly inhibition of glutathione reductase leading to oxidative damage

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15
Q

Excessive dietary intake of Zn interferes with absorption/utilization of these 2 elements?

A

copper and iron

–also antagonizes Cu/Fe in hemoglobin synthesis

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16
Q

Pathology of Zn toxicosis?

A

gastritis, gastric ulcers, liver damage, renal tubular casts, pancreatitis, decreased copper in liver in chronic toxicosis

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17
Q

What samples should you test when diagnosing Zn toxicosis?

A

serum, liver, kidney, pancreas, urine

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18
Q

Lab diagnosis of Zn toxicosis?

A

hemolytic anemia, icterus, hemoglobinuria, azotemia, hypercreatinemia, hyperphos
–use dark blue top tube (trace element detection)

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19
Q

Radiographs can be useful in diagnosing Zn toxicosis bc?

A

find metal foreign body in GIT

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20
Q

Differential diagnosis for Zn toxicosis?

A

Cu tox, napthalene tox, onion px, red maple leaf (horse), cotton seed (gossypol), mustard px, IMHA, hyperphosphatemia, DMSO overdose, guaifenesin overdose

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21
Q

Treatment of Zn toxicosis?

A

decon–>remove Zn FBs–emesis, endoscopy, sx, cathartics
supportive–>blood transfusion, O2 therapy, fluid therapy, tx of ARF, pancreatitis
chelation–>calcium disodium EDTA (after removal of source and correcting dehydration), D-penicillamine

22
Q

Sources of Fe toxicosis?

A

accidental ingestion of human oral supplements in pets, iatrogenic overdose in pigs/piglets

23
Q

Uses of iron?

A

oral supplements in humans/pets, mineral fortified fertilizers, some slug/snail baits, types of oxygen absorbing sachets–prevents spoilage, hand warming pads

24
Q

Name the different forms of iron.

A

elemental, ferrous–divalent, ferric–trivalent

25
Q

Organic Fe is ____ irritant and _____ astringent than inorganic Fe.

A

less and less

26
Q

Ferrous Fe is ____ irritant and _____ astringent than ferric.

A

less and less

27
Q

How can you calculate amount of elemental iron ingested?

A

multiply amount of iron salt by % elemental iron

28
Q

T/F Toxicity of Fe oral preps is greater than that of parenteral preps.

A

FALSE–parenteral preps more toxic than oral preps

29
Q

How can Fe toxicosis cause rickets in piglets?

A

> 5,000 ppm in diet can interfere with phosphate absorption

30
Q

ADME of iron?

A

A=ferrous iron abs in SI using energy dependent carrier mechanism–abs ferrous is oxidized to ferric iron
D=ferric iron binds to transferrin in plasma and distributed throughout
E=small amount of Fe excreted in urine

31
Q

T/F Excretion of iron in urine greatly increases during iron toxicosis.

A

FALSE–small amount of Fe excreted in urine does not significantly increase during toxicosis–homeostasis is via control of absorption of Fe

32
Q

What form of iron is absorbed from GI tract?

A

ferrous iron

33
Q

How is iron divvied up in the body?

A

70% in Hb, 10% in myoglobin, rest utilized in enzymes–perioxidase catalase, cytochrome C, or stored in liver, spleen and bones as hemosiderin or ferritin

34
Q

What is the primary transport protein for iron in blood?

A

transferrin

35
Q

____ iron is very reactive and causes direct cellular damage–with primary effects on GIT, liver, CV resulting in shock or death.

A

Free

36
Q

MOA of oral acute iron overdose?

A

direct corrosion of GI mucosa, V+, D+, fluid and electrolyte loss, systemic acidosis, shock

37
Q

MOA of circulating free iron?

A

accumulates in liver causing mitochondrial damage and liver damage, systemic acidosis, and shock. causes free radical lipid perioxidation/damage to membranes, increased vascular permeability, coagulopathy, vasodilation, CV collapse and shock.

38
Q

MOA of injectable iron overdose?

A

causes a peracute anaphylactoid rxn and very rapid death d/t histamine release

39
Q

Clinical signs of parenteral iron prep overdose?

A

peracute–>anaphylactoid rxn, shock, death w/in secs-mins

acute–> severe depression, shock, acidosis, death w/in hrs

40
Q

Clinical signs of oral iron prep overdose?

A

acute iron tox divided into 4 stages
1–>(0-6 hrs) nausea, V+, D+, GI hemorrhage
2–>(6-24 hrs) apparent recovery, GI signs resolve, animal is more alert–don’t fall for it!
3–>(12-96 hrs) most serious d/t metabolic effects–V+, D+, GI hem, met acidosis, coagulopathy, liver failure, CV collapse
4–>(2-6 wks) if survive stage 3, GI obstruction may be seen d/t fibrosing repair of GIT

41
Q

Pathology of parenteral iron prep overdose?

A

yellowish-brown discoloration at injection site and lymph nodes

42
Q

Pathology of oral iron prep overdose?

A

GI ulcers, hemorrhagic enteritis, congestion of liver/kidneys, liver necrosis, icterus, hemoglobinuria

43
Q

Lab diagnosis of iron toxicosis?

A

increased serum iron, increased total serum total iron binding capacity, increased PCV, acidosis, hemoglobinuria, abnormal rads

44
Q

Differential diagnosis of iron toxicosis?

A

agents that cause shock like signs–hemorrhage, hypotension, hemolysis, methemoglobinemia

45
Q

T/F Activated charcoal can be used as in decontamination of ingested iron.

A

FALSE–charcoal is not effective

46
Q

Treatment of iron toxicosis?

A

decon–>emesis, gastric lavage, milk of magnesia to precipitate iron–within 4 hrs of ingestion
supportive–>IV fluids for dehydration, acidosis, shock; GI protectant (sucralfate); anaphylactoid (epi, O2, antihistamines)
chelation–>desferoxamine by CRI–IM less effective–required for 2-3 days

47
Q

Prognosis of iron toxicosis?

A

good in animals treated early–guarded to poor in animals with severe signs

48
Q

When is desferoxamine indicated for treatment of iron toxicosis?

A

only in severe toxicosis w/in 12 hrs of ingestion

49
Q

Side effects of desferoxamine?

A

rapid injection causes hypotension, cardiac arrhythmias, pulmonary tox

50
Q

Urine will be _______ in color during treatment of iron toxicosis.

A

reddish-brown

51
Q

______ will help enhance excretion of iron.

A

oral ascorbic acid

52
Q

extra random info about iron!!

A

normally serum transferrin concentrations greatly exceed incoming iron. oral acute overdose overwhelms the selective abs mechanism and saturates ferritin in GI mucosal cells leading to abs of toxic concentrations of Fe–free Fe causes saturation of transferrin resulting in free circulating iron.

Toxicology Exam 2 (8 decks)

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