Fe, Zn, Mn, Flashcards
Iron
-essential trace mineral needed for hemoglobin, myoglobin, cytochrome enzymes
Sources of iron
Companion animals: iron supplement overdose, oxygen absorber packets, handwarmer packets, certain molluscicides
Large animals: excessive supplementation
Iron normal physiology
- Absorption of iron in small intestines
- binds to transferrin in blood
- transport to liver
- bone marrow for hemoglobin production and bound to ferritin for storage in liver, spleen, bone marrow
Iron mechanism of action
There is no active iron excretion mechanism therefore it accumulates
*transferrin binding is saturated resulting in lots of free iron and oxidative damage
Target= Liver
Clinical presentations of iron toxicity
- peracute toxicosis
- acute toxicosis
- chronic toxicosis
Peracute iron toxicosis
- common in neonatal pigs
-mins to hrs post exposure
-anaphylaxis, circulatory collapse, death
*animals are at a higher risk if vit E/Se deficient
Acute iron toxicosis
-within hours of post ingestion= vomiting with blood, diarrhea, melena, lethargy, abdominal pain
-6-24 hrs post exposure= temp improvement
-12-96hrs post exposure= depression, shock, CV collapse, liver failure
-death
Clinical pathology of acute iron toxicosis
-metabolic acidosis
-high liver enzymes
-coagulopathy
Chronic iron toxicosis
-progressive wasting, loss of condition
-dull mentation
-icterus, ascites
-rough hair coat
Clinical pathology of chronic iron toxicosis
-increased liver enzymes
-indicators of liver failure
-high %transferrin saturation
Gross pathology of chronic iron toxicosis
-hepatic fibrosis/cirrhosis
-brown discolouration of tissues
Hemosiderosis
Asymptomatic increase in iron deposition of tissues
-not pathologic process
-deposits in different organs normally
Hemochromatosis
Organ damage secondary to iron overdose
-can be hereditary for some species
-chronic iron toxicosis
-fibrotic change
Management of iron toxicity for peracute vs acute
-difficult to manage to peracute poisoning
-acute= antacids, activated charcoal, remove iron source, supportive care, monitoring
*Chelation therapy= deferoxamine
Management of chronic iron toxicity
-ID iron source
-supportive care
-consider chelation therapy
Diagnosis of iron toxicity
-radiographs, US
-measure tissue iron in serum
-measure liver iron concentration postmortem
Prognosis of iron toxicity
good if asymptomatic 6-8hrs post ingestion and early decontamination
*guarded with clinical signs and if iron serum is more than 500mcg/dL
Zinc
-essential trace mineral
-exposure: dietart indiscretion
Sources of Zn
-copper plated zinc pennies
-baby cream
-sunburn ointment
-toys/tags
-metals (zippers, nuts, bolts, wires)
-jewelry
-supplements
Zinc mechanism of action
Product contacts stomach acid which releases free Zn
*causes mucosal damage and oxidative damage= intravascular hemolysis
What does Zinc toxicity target?
-RBCs
-GI
-liver
-kidney
-pancreas
Zinc clinical signs
within mins to days
Phase 1: GI (vomiting, lethargy, ulcers, melena)
Phase 2: oxidative damage (intravascular hemolysis, anemia, acute kidney and liver failure, pancreatitis, tachycardia, pain)
*potentially could lead to DIC and neuro signs
Clinical pathology in Zinc toxicity phase 2
- intravascular hemolysis= hemoglobinemia, hemoglobinuria, ghost cells, icterus
- increased BUN, bilirubin, liver enzymes, lipase/amylase
- UA: proteinuria, hemoglobinuria, bilirubinuria, tubular casts
Management of Zn toxicity
-decontamination
-no antidote
-radiographs
-supportive care (antacids, fluids, gastroprotectants)
-retrieve source (gastroscopy, ex lap)
-chelation therapy
Zinc diagnosis
-history of foreign object ingestion
-hemolytic anemia
-Zn concentration in tissues
DDx for Zn toxicity
Any causes of oxidative anemia= onions/garlic, mothballs, acetaminophen, copper, snake bites
Prognosis of Zn
Dependent on severity of liver, kidney, pancreas involvement
*improvement noted within a few days of removal
Manganese
essential trace mineral= involved in macromolecule metabolism, enzymatic reactions as a co factor, bone/cartilage formation, reproduction
Manganese exposures in animals
Livestock= mixing errors
Companion animals= ingestion of joint supplements
Manganese mechanism of toxicity
mechanism unknown- potentially oxidative damage
*targets Liver
Species sensitivity of manganese
Dogs most sensitive
*likely linked with low nutritional requirement
Manganese clinical signs
Onset within several hours
GI: vomiting, anorexia, lethargy, diarrhea, melena
Liver damage: high liver enzymes, onset of acute liver failure, icterus and distended abdomen
Manganese management
-no antidote
-symptomatic and supportive care (fluids, gastroprotectants, hepatoprotectants, anti emetics
-manage coagulopathy
-chelation
Manganese diagnosis
-history of ingestion
-detection in tissues (blood antemortem; liver and kidneys post mortem)
-liver histopathology= Rhodanine staining
Molybdenum
Essential trace element
-all species easily meet needs
-sources: soils, mining industry contaminations, fertilizers
Molybdenum species susceptibility
Cattle> sheep> goats» monogastrics
Clinical signs of Molybdenum toxicity
- secondary copper deficiency
- enzootic ataxia (swayback) in sheep and goats
Secondary copper deficiency from molybdenum toxicity
-Molybdenum interacts with dietary sulfur and copper= thiomolybdates
*leads to diarrhea, anorexia, red tinge to black hair coats, depigmentation around eyes, poor reproduction efficiency, anemia
Enzootic ataxia
-Ewes and nannies are copper deficient affecting lambs and kids by decreasing myelin formation and demyelination at birth
Congenital enzootic ataxia
stillborn, weak, unable to stand, spastic tetraparalysis
*die within first week of life
Delayed onset of molybdenum
Slower progression; 2-4mths
-hindlimb ataxia progressing to forelimbs, recumbency, and death
Management of molybdenum toxicity
-copper supplements (ideally 6:1 - 10:1
- no cute or treatment for enzootic ataxia
Diagnosis of molybdenum toxicity
-high blood Molybdenum and low Copper
-feed and water testing for molybdenum and sulfur
