Zinc & Iron Flashcards
In what environments are zinc salts formed?
Acidic environments
Is there a good excretion mechanism for zinc? why or why not?
No there is not bc it is an essential mineral
What sources of zinc are animals exposed to?
Accidental ingestion of pennies, galvanized wires, plumbing nuts, batteries, zinc oxide skin ointment/lotions/medication
What is the acute, subacute, and chronic LD50 of zinc in dogs?
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
What environment will increase zinc release?
Acidic environment increased release and formation of caustic zinc salts
T/F: Zinc undergoes enterohepatic circulation and conservation
TRUE
30-40% extracted from the liver - returns back to circulation via bile, small intestine, and absorption
**zinc is highly conserved
How is zinc transported in the blood to the liver?
Bound to plasma proteins - albumin and globulins
What are the major organs/tissues affected by zinc toxicosis?
RBC = intravascular hemolysis***
kidney
liver
pancreas
What is the MOA of zinc mediated hemolysis?
Direct damage to RBC cell membranes, damage to RBC organelles, immune mediated destruction, inhibition of specific RBC biochemical mechanisms
Is zinc mediated renal injury a secondary or primary process?
Secondary: renal damage will occur due to anemia, hypoxia, or hemoglobinurea
but
zinc may directly injury the renal tubular epithelium
Where does the most rapid accumulation and turnover of zinc occur?
Pancreas liver kidney spleen male repro
What is the major organ of zinc metabolism?
Liver
metallothionein sequesters metal ions for excretion
glutathione sequesters free radicals associated with zinc toxicity
What is the primary site of zinc excretion?
feces via bile and pancreatic juices
only about 10% is excreted in the urine
Excessive dietary zinc intake can interfere with the absorption and utilization of what minerals?
Copper and Iron
*antagonizes copper and iron in hemoglobin synthesis
T/F: Zinc toxicosis can be seen as an acute, subacute, or chronic form
TRUE
What GI clinical signs are associated with zinc toxicosis?
Vomiting, anorexia, lethargy, abdominal pain, dhr, and pica
What renal associated clinical signs can be seen with zinc toxicosis?
Azotemia (elevated BUN), hyperphosphatemia
What clinical signs may you see in cattle and foals with zinc toxicosis?
livestock will show decreased weight gain or milk production
lameness and stiffness is prominent in foals
What lesions are characteristic of zinc toxicosis?
Gastritis, GI ulcers, renal tubular casts, liver damage, pancreatitis
What special tubes should be used for chemical analysis of zinc?
Trace element tubes (royal/dark blue tops) **avoid contamination with zinc stearate
Can test: serum, liver, kidney, pancreas, urine
What are the major lab findings associated with zinc toxicosis?
Hemolytic anemia, hemoglobinuria, azotemia, hyperphosphatemia, +/- evidence of pancreatitis
Why should abdominal radiographs be taken in an animal suspected of zinc toxicosis?
To look for a FB - often will have a metal FB
What tx is recommended for zinc toxicosis?
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
Is chelation therapy recommended for zinc toxicosis?
should be avoided
Chelation treatment may INCREASE zinc redistribution and absorption from the intestines and cause further damage.
What is the prognosis of a dog with a zinc related FB?
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
What iron state is in the hemoglobin and myoglobin?
Ferrous (Fe2+) - divalent
and up to 25% is ferric (Fe3+) - trivalent
Hemosiderin, ferritin, and transferrin do what with iron?
iron binding, transport, and storage
Where is Ferric iron stored?
Liver
spleen
bone marrow
What sources of iron are pets exposed to in cases of toxicosis?
oral iron supplements, fertilizers, slug/snail bait
**parental iron preparations - overdose in piglets
What form of iron has the highest toxicity risk?
Soluble salts
What is the most toxic source of exposure of iron?
Intravenous = most toxic
Injectable: iron dextran - newborn pigs (150-200ppm)
Orally = least toxic. Has caustic effect on the GIT and acidity
What are major causes of iron deficiency in piglets?
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
What mineral or vitamin deficiency in pregnant sows will increase the risk of iron toxicity in piglets (after their iron supplementation)?
Selenium and Vitamin E deficiency of the sow
What form of iron is involved in the formation of free radicals?
Free iron ions***
they can change from ferrous to ferric rapidly
excess free radicals = cellular damage
Which is more irritating, Ferrous or ferric iron?
Ferric (Fe3+) > Ferrous (Fe2+)
*organic iron is LESS irritant than inorganic salt
What value must be determined when assessing the potential toxicity of an iron overdose?
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
T/F: Most animals have an efficient mechanism of iron excretion
FALSE
this is a highly conserved mineral so the mechanism of excretion is not great
Iron from hemoglobin degradation is rapidly bound to _____ and transported to bone marrow for re-synthesis of hemoglobin
Transferrin = primary plasma transport protein
normally serum transferrin concentrations greatly exceed incoming iron
What is the MOA of iron toxicosis?
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
How is iron homeostasis controlled in the body?
via control of absorption since there is no good excretion mechanism
Where does the primary effect of iron toxicosis take place?
CV system
GIT
Liver
leading to shock and death
What CV damage is the result of excessive iron?
Fatty necrosis of the myocardium, post arteriolar dilation, increased capillary permeability, and reduced CO
What GIT damage is the result of excessive iron?
direct corrosion of the GIT mucosa, vomiting, dhr, fluid/lyte loss, systemic acidosis and shock
What damage is done to the liver if there is excessive free iron in circulation?
mitochondrial damage, liver damage, systemic acidosis
What clinical signs are associated with acute iron toxicosis due to an injection?
May see anaphylactic reaction or shock and death within a few minutes
or
severe depression, shock, acidosis. death within hours
How many stages of iron toxicity are there?
Five - according to the dose and duration of iron ingested
What lesions are seen with iron toxicosis from parental preparations?
Yellow-brown discoloration at injection sites
What lesions are seen with iron toxicosis from oral preparations?
GIT ulcerations and hemorrhagic enteritis
congestion of the liver, kidney, liver necrosis, icterus, hemoglobinuria
What will the transferrin saturation and serum total iron binding capacity values be in a patient with iron toxicosis?
Increased transferrin saturation
Low serum total iron binding capacity
How soon after ingestion must GIT decontamination occur for a good prognosis associated with oral iron toxicosis.
effective within 4 hrs of ingestion
should induce emesis or perform gastric lavage prior to onset of clinical signs
What can be used to precipitate iron in the GIT?
Milk of magnesia
Is chelation therapy indicated for iron toxicosis?
Only in severe cases within 12 hours of iron ingestion
deferoxamine (Desferal)
