26 – Iron, Zinc, Manganese, Molybdenum

Question 1

Iron

Answer 1

• Essential trace mineral
• Sources:
  o Large animals: excessive supplementation
  o Companion: overdose, oxygen absorber packets, handwarmer packets

Question 2

Iron: mechanism of action

Answer 2

1. Absorption into SI
2. Binds to transferrin in blood
3. Transport to liver
4. Bone marrow for hemoglobin production and bound to ferritin for storage in liver, spleen, bone marrow
   *no active excretion mechanism=accumulates
   *free iron=causes oxidative damage

Question 3

*Iron: target organ

Answer 3

• LIVER

Question 4

*Iron: peracute toxicosis

Answer 4

• Neonatal pigs
• Minutes to hours post-exposure
• Resembles anaphylaxis
  o No liver involvement at this stage
• Circulatory collapse, death
• Higher risk: vit E/Se deficient

Question 5

*Iron: acute toxicosis

Answer 5

• Within several hours post-ingestion
• 6-24hrs post-exposure: temporary improvement
• 12-96hrs post-exposure: depression, shock/CV collapse, liver failure
  o Acute renal failure secondary to shock
• Death possible
• Clin path: metabolic acidosis (elevated liver enzymes, coagulopathy)

Question 6

*Iron: chronic toxicosis

Answer 6

• Progressive wasting, loss of condition
• Dull mentation
• Icterus, ascites
• Rough hair coats
• Clin path: increased liver enzymes, indicators of liver failure, elevated % transferring saturation)

Question 7

What is the gross pathology of chronic iron toxicosis?

Answer 7

• Hepatic fibrosis/cirrhosis
• Brown discolouration of tissues

Question 8

Hemosiderosis=secondary iron overload

Answer 8

• Asymptomatic increase in Fe deposition in tissues

Question 9

**Hemochromatosis

Answer 9

• Organ damage secondary to iron overdose
• Hereditary for some species (Salers cattle)
• Chronic iron toxicosis
• Fibrotic change

Question 10

Iron management: acute poisoning

Answer 10

• (difficult to manage peracute)
• If asymptomatic: antacids
  o *NO activated charcoal as it is a metal
• Remove source of iron
• Symptomatic and supportive care
• *chelation therapy: DEFEROXAMINE (human medication)
• Frequent monitoring

Question 11

Iron management: chronic poisoning

Answer 11

• ID source of iron
• Mostly supportive care
• Consider chelation therapy (Deferoxamine)
  o Maybe more so with secondary?

Question 12

Iron diagnosis

Answer 12

• Radiographs, ultrasound
• Measure tissue iron
  o Antemortem: serum iron and total iron binding capacity
   Hemolysis will falsely increase IRON
   Serum iron decreased with: hypoproteinemia, inflammation, hypothyroidism, kidney disease
  o Postmortem: liver iron concentration

Question 13

Iron prognosis

Answer 13

• Good if asymptomatic 6-8hrs post ingestion and early decontamination
• Guarded with clinical signs (esp. if serum iron Is >500mcg/dL)

Question 14

Zinc

Answer 14

• Essential trace mineral
• Many sources
  o Pennies
  o White baby cream
  o Sunburn ointment
  o Large animals: excessive administration or chewing on galvanized metal

Question 15

*Zinc: EXPOSURE SCENARIO

Answer 15

• DIETARY INDISCRETION

Question 16

Zinc: mechanism of action

Answer 16

• Contact with stomach acid=release of free zinc
  o Caustic=mucosal damage
  o Oxidative damage=intravascular hemolysis

Question 17

**Zinc: target organs

Answer 17

• RBCs
• GI
• LIVER
• KIDNEY
• PANCREAS

Question 18

*Zinc: clinical features

Answer 18

• *PHASE 1: GI signs
  o Nausea, vomiting, diarrhea, anorexia, lethargy
  o Ulcers, hematemesis, melena
• *PHASE 2: widespread oxidative damage
  o Intravascular hemolysis, oxidative damage hemolytic anemia, acute kidney/liver failure, pancreatitis
  o Abdominal pain, tachycardia, icterus
• Risk for development of acute kidney or liver failure, DIC, neuro involvement

Question 19

*Zinc phase 2: clinical pathology

Answer 19

• Intravascular hemolysis: hemoglobinemia (increased MCHC), hemoglobinuria, Ghost cells, icterus, spherocytes, Heinz bodies
• Chem: increase BUN/bilirubin, increased liver enzymes, increased lipase/amylase
• UA: proteinuria, hemoglobinuria, bilirubinuria, tubular casts

Question 20

Zinc: gross necropsy

Answer 20

• Source
• GI erosion, ulceration
• Icterus
• Hepatomegaly, splenomegaly

Question 21

Zinc: histology

Answer 21

• Liver: centrilobular to diffuse hepatic necrosis
• Kidney: tubular degeneration and tubular epithelial necrosis
• Pancreas: necrosis, fibrosis

Question 22

Zinc management

Answer 22

• No specific antidote
• Radiographs
• Supportive care for hemolytic anemia, GIT, liver, kidneys
  o *ANTACIDS: to help slow down the release of Zn
  o Pain management
  o Antiemetics, hepatoprotectants, fluids
• RETRIEVE THE SOURCE: gastroscopy, exploratory laparotomy
• Can consider chelation therapy (but no specific one)

Question 23

Zinc diagnosis

Answer 23

• History of foreign object
• Hemolytic anemia (coombs negative)
• Radiographs, abdominal ultrasound
• Zn concentration in tissues
  o Major caveat: zinc can become falsely elevated in serum due to hemolysis, steroid administration, contamination from tubes

Question 24

Zinc prognosis

Answer 24

• Dependent on severity of liver, kidney and pancreas involvement
• Improvement noted within a few days of removal

Question 25

Manganese

Answer 25

- Essential trace mineral o Bone and cartilage formation o Reproduction o Highest concentrations in bone, liver, kidney - Chronic poisoning in humans: manganism - Vet poisonings o Extremely rare in livestock: mixing errors o Companion animals: ingestion of JOINT SUPPLEMENTS

Question 26

Manganese mechanism of toxicity

Answer 26

- Dogs seem to be more sensitive o Low nutritional requirement - Not fully understood: maybe oxidative damage

Question 27

*Manganese: target organ

Answer 27

- LIVER

Question 28

Manganese clinical features

Answer 28

- GI: vomiting, anorexia, lethargy, diarrhea, melena - Liver damage o Elevated liver enzymes o Onset of acute liver failure o Icterus, distended abdomen

Question 29

Manganese: management

Answer 29

- No specific antidote - Symptomatic and supportive care - Management of metabolic derangements and coagulopathy - Therapeutic plasma exchange - Urosidol, cholestyramine, iron, chelation (para-amionosalicyclic acids)

Question 30

Manganese: diagnosis

Answer 30

- History of ingestion or other manganese containing products - Detection in tissues o Antemortem: whole blood o Post mortem: liver, kidneys - Supported by liver histopathology o Rhodamine staining

Question 31

Molybdenum

Answer 31

- Essential trace element - Sources: high soils, contamination from mining industries, some fertilizers - All species easily meet dietary requirements

Question 32

Molybdenum: susceptibility

Answer 32

- Cattle > sheep > goats >>> monogastrics

Question 33

*Molybdenum: SECONDARY COPPER DEFICIENCY

Answer 33

- Get complexes and Cu can not be absorbed - Feed ratio 2:1 Cu:Mo - *common in western Canada - Progressive herd-level changes o Diarrhea, anorexia, thriftiness, poor BCS o Red tinge to black hair coats, depigmentation around eyes, poor wool condition o Poor reproductive efficiency o Anemia

Question 34

Molybdenum: ENZOOTIC ATAXIA (“swayback), sheep and goats

Answer 34

- Ewes and nannies are copper deficient: affects lambs and kids - Decreased myelin formation and demyelination - Congenital: stillborn, weak, unable to stand to nurse, spastic tetra paralysis - *inadequate immune system - Delayed onset: slower progression o 2-4 months old o Hindlimb ataxia and progressing to forelimbs o Recumbency and death

Question 35

Molybdenum: management

Answer 35

- Copper supplementation o Ideal feed ration: 6:1 to 10:1 o Be careful with sheep and goats - No cure or treatment with enzootic ataxia

Question 36

Molybdenum: diagnosis

Answer 36

- Elevated blood Mo +/- decreased Cu - Feed and water testing for Mo, sulfur (sulfate)