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ToxFall17 COPY for AeJ > Zinc & Iron > Flashcards

Zinc & Iron Flashcards

1
Q

In what environments are zinc salts formed?

A

Acidic environments

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2
Q

Is there a good excretion mechanism for zinc? why or why not?

A

No there is not bc it is an essential mineral

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3
Q

What sources of zinc are animals exposed to?

A

Accidental ingestion of pennies, galvanized wires, plumbing nuts, batteries, zinc oxide skin ointment/lotions/medication

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4
Q

What is the acute, subacute, and chronic LD50 of zinc in dogs?

A

Acute: LD50 = 100mg/kg zinc salts

Subacute = ~5 pennies = 12,200mg

Chronic: caused by exceeding 2000 ppm in the diet over time

*dogs normal diet ranges from 80 - 120 ppm

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5
Q

What environment will increase zinc release?

A

Acidic environment increased release and formation of caustic zinc salts

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6
Q

T/F: Zinc undergoes enterohepatic circulation and conservation

A

TRUE

30-40% extracted from the liver - returns back to circulation via bile, small intestine, and absorption

**zinc is highly conserved

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7
Q

How is zinc transported in the blood to the liver?

A

Bound to plasma proteins - albumin and globulins

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8
Q

What are the major organs/tissues affected by zinc toxicosis?

A

RBC = intravascular hemolysis***
kidney
liver
pancreas

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9
Q

What is the MOA of zinc mediated hemolysis?

A

Direct damage to RBC cell membranes, damage to RBC organelles, immune mediated destruction, inhibition of specific RBC biochemical mechanisms

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10
Q

Is zinc mediated renal injury a secondary or primary process?

A

Secondary: renal damage will occur due to anemia, hypoxia, or hemoglobinurea

but

zinc may directly injury the renal tubular epithelium

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11
Q

Where does the most rapid accumulation and turnover of zinc occur?

A 
Pancreas
liver
kidney
spleen
male repro
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12
Q

What is the major organ of zinc metabolism?

A

Liver

metallothionein sequesters metal ions for excretion

glutathione sequesters free radicals associated with zinc toxicity

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13
Q

What is the primary site of zinc excretion?

A

feces via bile and pancreatic juices

only about 10% is excreted in the urine

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14
Q

Excessive dietary zinc intake can interfere with the absorption and utilization of what minerals?

A

Copper and Iron

*antagonizes copper and iron in hemoglobin synthesis

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15
Q

T/F: Zinc toxicosis can be seen as an acute, subacute, or chronic form

A

TRUE

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16
Q

What GI clinical signs are associated with zinc toxicosis?

A

Vomiting, anorexia, lethargy, abdominal pain, dhr, and pica

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17
Q

What renal associated clinical signs can be seen with zinc toxicosis?

A

Azotemia (elevated BUN), hyperphosphatemia

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18
Q

What clinical signs may you see in cattle and foals with zinc toxicosis?

A

livestock will show decreased weight gain or milk production

lameness and stiffness is prominent in foals

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19
Q

What lesions are characteristic of zinc toxicosis?

A

Gastritis, GI ulcers, renal tubular casts, liver damage, pancreatitis

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20
Q

What special tubes should be used for chemical analysis of zinc?

A

Trace element tubes (royal/dark blue tops) **avoid contamination with zinc stearate

Can test: serum, liver, kidney, pancreas, urine

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21
Q

What are the major lab findings associated with zinc toxicosis?

A

Hemolytic anemia, hemoglobinuria, azotemia, hyperphosphatemia, +/- evidence of pancreatitis

22
Q

Why should abdominal radiographs be taken in an animal suspected of zinc toxicosis?

A

To look for a FB - often will have a metal FB

23
Q

What tx is recommended for zinc toxicosis?

A

Remove any zinc related FB, induce emesis vs endoscopy vs sx

Cathartics

Supportive care: IVF, blood transfusion, O2, tx of renal failure and or pancreatitis

24
Q

Is chelation therapy recommended for zinc toxicosis?

A

should be avoided

Chelation treatment may INCREASE zinc redistribution and absorption from the intestines and cause further damage.

25
Q

What is the prognosis of a dog with a zinc related FB?

A

In canines with zinc levels dropped quickly after the FB was removed

good - early dx and tx

Guarded to poor if patient has severe hemolytic anemia

26
Q

What iron state is in the hemoglobin and myoglobin?

A

Ferrous (Fe2+) - divalent

and up to 25% is ferric (Fe3+) - trivalent

27
Q

Hemosiderin, ferritin, and transferrin do what with iron?

A

iron binding, transport, and storage

28
Q

Where is Ferric iron stored?

A

Liver
spleen
bone marrow

29
Q

What sources of iron are pets exposed to in cases of toxicosis?

A

oral iron supplements, fertilizers, slug/snail bait

**parental iron preparations - overdose in piglets

30
Q

What form of iron has the highest toxicity risk?

A

Soluble salts

31
Q

What is the most toxic source of exposure of iron?

A

Intravenous = most toxic

Injectable: iron dextran - newborn pigs (150-200ppm)

Orally = least toxic. Has caustic effect on the GIT and acidity

32
Q

What are major causes of iron deficiency in piglets?

A

Rapid growth of the nursing piglet and low iron content in the sows colostrum and milk

Tx: IM or SQ iron dextran 2-3 days post birth

33
Q

What mineral or vitamin deficiency in pregnant sows will increase the risk of iron toxicity in piglets (after their iron supplementation)?

A

Selenium and Vitamin E deficiency of the sow

34
Q

What form of iron is involved in the formation of free radicals?

A

Free iron ions***

they can change from ferrous to ferric rapidly

excess free radicals = cellular damage

35
Q

Which is more irritating, Ferrous or ferric iron?

A

Ferric (Fe3+) > Ferrous (Fe2+)

*organic iron is LESS irritant than inorganic salt

36
Q

What value must be determined when assessing the potential toxicity of an iron overdose?

A

The amount of elemental iron in the supplement

Ex: 200mg of iron salt (ferrous carbonate) is ingested with 48% elemental iron

200mg X 0.48 = 96 mg elemental iron

37
Q

T/F: Most animals have an efficient mechanism of iron excretion

A

FALSE

this is a highly conserved mineral so the mechanism of excretion is not great

38
Q

Iron from hemoglobin degradation is rapidly bound to _____ and transported to bone marrow for re-synthesis of hemoglobin

A

Transferrin = primary plasma transport protein

normally serum transferrin concentrations greatly exceed incoming iron

39
Q

What is the MOA of iron toxicosis?

A

Acute: high iron will overwhelm the selective absorption mechanism and saturate ferritin in the GI mucosal cells leading to absorption of toxic concentrations of free iron

*circulating free iron ions will form free radicals –> Cellular damage

40
Q

How is iron homeostasis controlled in the body?

A

via control of absorption since there is no good excretion mechanism

41
Q

Where does the primary effect of iron toxicosis take place?

A

CV system
GIT
Liver

leading to shock and death

42
Q

What CV damage is the result of excessive iron?

A

Fatty necrosis of the myocardium, post arteriolar dilation, increased capillary permeability, and reduced CO

43
Q

What GIT damage is the result of excessive iron?

A

direct corrosion of the GIT mucosa, vomiting, dhr, fluid/lyte loss, systemic acidosis and shock

44
Q

What damage is done to the liver if there is excessive free iron in circulation?

A

mitochondrial damage, liver damage, systemic acidosis

45
Q

What clinical signs are associated with acute iron toxicosis due to an injection?

A

May see anaphylactic reaction or shock and death within a few minutes

or

severe depression, shock, acidosis. death within hours

46
Q

How many stages of iron toxicity are there?

A

Five - according to the dose and duration of iron ingested

47
Q

What lesions are seen with iron toxicosis from parental preparations?

A

Yellow-brown discoloration at injection sites

48
Q

What lesions are seen with iron toxicosis from oral preparations?

A

GIT ulcerations and hemorrhagic enteritis

congestion of the liver, kidney, liver necrosis, icterus, hemoglobinuria

49
Q

What will the transferrin saturation and serum total iron binding capacity values be in a patient with iron toxicosis?

A

Increased transferrin saturation

Low serum total iron binding capacity

50
Q

How soon after ingestion must GIT decontamination occur for a good prognosis associated with oral iron toxicosis.

A

effective within 4 hrs of ingestion

should induce emesis or perform gastric lavage prior to onset of clinical signs

51
Q

What can be used to precipitate iron in the GIT?

A

Milk of magnesia

52
Q

Is chelation therapy indicated for iron toxicosis?

A

Only in severe cases within 12 hours of iron ingestion

deferoxamine (Desferal)

ToxFall17 COPY for AeJ (38 decks)

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