iron, zinc, mg, mn Flashcards
sources of iron
- Companion animals: iron supplement overdose, oxygen absorber packets,
handwarmer packets, certain molluscicides - Large animals: excessive supplementation
Toxicity
* Mild GI signs: 5-20 mg/kg
* GI and liver: 20-60 mg/kg
* Potentially fatal: 100-250 mg/kg
iron mechanism of action and target organ
- There is no active iron excretion mechanism → accumulates
- Toxicosis: transferrin binding is saturated → free iron-> Oxidative damage – lipid peroxidation
- Target organ: liver
iron clinical features 3 types
1 peracute toxicosis
2 acute toxicosis
3 chronic toxicosis
I R O N – C L I N I C A L F E A T U R E S
1. Peracute toxicosis
- Neonatal pigs
- Minutes to hours post-exposure
- Resembles anaphylaxis
- Circulatory collapse, death
- Higher risk: vitamin E/Se deficien
I R O N – C L I N I C A L F E A T U R E S
2. Acute toxicosis
Within several hours post-ingestion
* GI: vomiting/hematemesis, diarrhea/melena/hematochezia, lethargy, abdominal pain
* 6-24 hours post-exposure: temporary improvement
* 12-96 hours post exposure: depression, shock/cardiovascular collapse, liver failure
* Acute renal failure secondary to shock
* Death
* Clinical pathology: Metabolic acidosis
* Elevated liver enzymes
* Coagulopathy
I R O N – C L I N I C A L F E A T U R E S
3. Chronic toxicosis
Progressive wasting, loss of condition
* Dull mentation
* Icterus, ascites
* Rough hair coats
* Clinical pathology
* Increased liver enzymes
* Indicators of liver failure
Gross pathology: hepatic fibrosis/cirrhosis, brown discolouration of tissues
Hemochromatosis
-organ damage secondary to iron overdose
* Hereditary for some species (Salers cattle)
* Chronic iron toxicosis
* Fibrotic change
iron management
- Difficult to manage peracute poisoning
- Acute poisoning:
- If asymptomatic: antacids (MgOH, CaCO3)
- Remove source of iron: gastroscopy, endoscopy, enema
-activated charcoal**NO SINCE ITS METAL - Symptomatic and supportive care: gastroprotectants
- Chelation therapy: deferoxamin**
chronic poisoning:
-identify source and remove
-supportive care
iron diagnosis
Radiographs, ultrasound
* Measure tissue iron
* Antemortem: serum iron + total iron binding capacity (TIBC) dont use hemolysed blood
postmortem: liver iron concentration
zinc sources
- Many sources of zinc
- Pennies are copper plated zinc, baby cream, toys
- Large animals: excessive administration, chewing on galvanized metal
- Exposure scenario: dietary indiscretion**
zinc mechanism of action + target
- Toxicity: approx. 100 mg/kg BW for most species
- Contact with stomach acid: release of free zinc
- Caustic → mucosal damage
- Oxidative damage → intravascular hemolysis
- Target organs: multiple → RBCs, GI, liver, kidney, pancrease
zinc clinical features
- Onset: variable – within minutes to days
- Phase 1: gastrointestinal signs**
- Nausea, vomiting, diarrhea, anorexia, lethargy
- Ulcers, hematemesis, melena
- Phase 2: widespread oxidative damage**
- Intravascular hemolysis, oxidative damage hemolytic anemia, acute kidney/liver failure, pancreatitis
- Abdominal pain, tachycardia, icterus
phase 2 zinc poisoning clin path
- Intravascular hemolysis: hemoglobinemia (↑ MCHC), hemoglobinuria, Ghost cells, icterus
- Chem: ↑ BUN/bilirubin, ↑ liver enzymes, ↑ lipase/amylase
- UA: proteinuria, hemoglobinuria
- Risk for development of acute kidney or liver failure, DIC, neuro involvement
zinc management
- No specific antidote
- Radiographs
- Supportive care of hemolytic anemia, GIT, liver, kidneys
- Antiemetics, gastroprotectants, hepatoprotectants, fluids,
transfusion products, antacids** - Pain management
- Retrieve the source**: gastroscopy, exploratory laparotomy
- Chelation therapy
zinc diagnosis and DDX
-diagnosis: history of foreign object ingestion, hemolytic anemia (Coombs negative)
* Radiographs (pre- and post-retrieval), abdominal ultrasound
* Zn concentration in tissues
* Major caveat: zinc can become falsely in serum elevated due to hemolysis, steroid administration, contamination from tubes
DDx: oxidative damage hemolytic anemia → onions/garlic
manganese toxicity, target
- Veterinary poisonings
- Extremely rare in livestock: mixing errors
- Companion animals: ingestion of joint supplement
-target organ: liver
magnesia clinical + management
- Onset: within several hours
- GI: vomiting, anorexia, lethargy, diarrhea, melena
- Liver damage
- Elevated liver enzymes
management: supportive and symptomatic care
Molybdenum mechanism
- Susceptibility: cattle > sheep > goats»_space; monogastrics
-leads to secondary copper deficiency**
Progressive herd-level changes
* Diarrhea, anorexia, unthriftiness, poor BCS
* Red tinge to black hair coat
-anemia
molybdenum clinical in sheep + goats
enzootic ataxia (“swayback”)**
* Ewes and nannies are copper deficient → affects lambs and kids
* Decreased myelin formation + demyelination
- Congenital: stillborn, weak, unable to stand to nurse, spastic tetraparalysis, die in 1 week
- Delayed onset: slower progression
- 2-4 months old
- Hindlimb ataxia progressing to forelimbs
-recumbency and death
molybdenum management and diagnosis
- Management
- Copper supplementation
- Ideal feed ratio: 6:1 – 10:1
- Diagnosis
- Elevated blood Mo ± decreased Cu
- Feed and water testing for Mo, sulfur (sulfate)
