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55 Cards in this Set

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__A__ is a by-product of Silver smelting.

__B__ comes from the melting of Copper and Tin.

__C__ is associated with ZnCarbonate as a contaminant
A. Lead

B. Arsenic

C. Cadmium
How do metals typically affect organisms?
Usually affect multiple organ systems - but a low doses, it will primarily affect a specific organ
Blood/Urine concentrations usually correlate best with?
Recent Exposure and Acute Effects

*except urinary Cadmium --- may reflect renal damage related to ACCUMULATIONS of Cd in kidney
Can the same metal have different toxicities in different situations?
Yes - whether the metal is organic or inorganic may affect how it interacts with your enzymes and membranes.
**eg Organic Hg (fish) is a primary Neurotoxin -- but Mercuric Chloride is Nephrotoxic.
Toxic metals and Essential metals have some interplay:

A. What metals use the same homeostatic mechanisms?
B. What metals have an inverse relationship with protein intake?
C. What affect does Vitamin C have on metals?
D. What metal interferes with Ca-dependent NT release?
A. Pb, Ca, Fe

B. Pb, Cd

C. increases Fe, decreases Pb, Cd

D. Pb
What protein binds Cd, Cu, Hg, Ag, and Zn?

What binds Ferric Iron in plasma?

What stores Ferrous Iron in tissues?
Metallothioneins

Transferrin (also carries Al, Mn)

Ferritin (liver, spleen, bone)
so then...how does that Ferric (3+) Iron become Ferrous (2+) Iron?
Ceruloplasmin
a Cu-containing oxidase
Define
A. Complexation
B. **Chelation** (clinical)
A. formation of a metal ion complex in which the metal ion is assoc.w/ an e- donor ligand

B. formation of ring structures consisting of the metal ion and TWO ligand atoms - **more excretable form, get the metal out of the system
Chelators:

BAL
British Anti-Lewisite
(2,3-dimercaptopropanol)

Adjunctive Tx w/ Lead Encephalopathy. Also pulls Lead off of RBCs

Adverse: vomit, tremor, coma, death
Chelators:

DMSA
an analog of BAL

given Orally! also removes Lead from soft tissues..though does not get to brain-lead.
Chelators:

EDTA
always use CALCIUM-EDTA (Na-EDTA will cause hypocalcemia)
given Parenterally
binds Lead and displaces with Ca
not effective for brain-lead.

Adverse: nephrotoxic
Trivalent Arsenic
inhibits cell respiration (so tissue w/high E reqs /actively dividing are most affected)

affect capillary integrity

10x more toxic than Pentavalent
Arsenic
effects who?
signs?
gah Cats! >horses>rums>swine>birds

severe GI signs - vomit, pain, weakness, ataxia, recumbent, weak --> SHOCK
*kidney damage

**though some organic forms may target the CNS
Arsenic - Tx for acute toxicosis?
Dimercaprol (BAL)
Succimer (DMSuccinicAcid)
*Supportive Care
Lead
A. where is it distributed?
B. mechanism?
A. More than 90% of absorbed lead is bound to RBCs
B. binds sulfhydryl groups -> inactivates enzymes of heme synth
also damages Na/K pumps -> ***RBC damage and Kidney Damage***
Lead
worse for young or adult?
absorption enhanced by deficiencies in?
Young (like with most toxins)

Ca, Zn, Fe, VitD
Lead

Clinical Signs
(Rums, Equids, Carnivores, Psittacines, Fowl/Raptors)
Rums - CNS
Horses - Peripheral Neuropathy
Dog/Cat - GI and neurologic
Psittacines - GI, neuro, renal
Fowl/Raprots - Chronic Wasting
Clin Path Hallmarks of Pb-toxicosis
Basophilic Stippling
Large numbers of Nucleated RBCs
Anemia (w/chronic exposure)
True or False

Whole Blood Lead Levels are indicative of severity of clinical signs.
FALSE
blood level does not reflect whole body burden.

However - in general, >0.3 is significant and >0.6 is typically toxicosis.
Lead / General Heavy Metal Tx:

What is a BIG rule for Chelation Therapy?
besides DMSA (Succimer)

do NOT give Chelators until the Metal has been removed from the GI tract!! You may increase absorption of the metal if it is still in the lumen.
Mercury
not too common anymore - we've taken it out of all products, but it still pops up every once in awhile when an animal ingests an obsolete product.
is playing with Mercury thermometers bad?
actually...not really... in fact, eating it isn't too bad either (or a broken thermometer in the rectum)

**the problem is the VOLATILE form
so what are the concerns then with Mercury?
ORGANIC
methyl/ethyl forms are Lipophilic and readily absorbed. --Kidney
Alkyl forms cross BBB
All forms cross Placenta (fetus gets cerebellar hypoplasia)
how nasty is a mercury spill in the dolphin tank?
Marine mammals appear to have some ability to detoxify mercury!!
Mercury Toxicosis -- Tx?
Acute - Egg Whites (protein to bind with and pass out)
Cathartics (sorbitol)
DMSA (Succimer)
supplement Se and VitE
so what's the deal with Mercury in Tuna?
Irreversible Neurotoxicosis - beware!!
Hg contamination in fish is a big concern!
Selenium... what does it cause?
needs to be a HIGH HIGH dose

embryo (missing whole body parts) in aquatic birds
FPSP - Focal Porcine Symmetrical Poliomyelomalacia
Selenium Dx?
garlicky breath (but don't hang your hat on this)
go with signs --- hindlimb ataxia progressing to tetraparesis -- separation of hoof at coronary band
DDx for Selenium?
There are a ton!! Tough one, BOLO for many other diseases/toxicities.
Copper

4 main ways Sheep suffer from Cu Toxicity.
1. Fed Calf/Horse diet --> Excessive Dietary Cu

2. on Monensin --> increases absorption

3. drank from the footbath

4. Mo deficiency causes increased absorption of Cu
Where is Cu absorbed - and where does it go in the body?
monogastric - stomach and SI
rums - lower SI

Copper transported to enterocytes -> albumin/ceruloplasmin/transcuprein -> LIVER and KIDNEY and brain
How does it cause damage?
Liver can hold a lot --- but when you hit threshold - Liver Necrosis --> massive flood of Copper into bloodstream
*erythrolysis, hemoglobinuria, high serum Cu
--> THEN it accumulates in the Kidneys (end-stage) --> Gun Metal Black Kidneys
Toxic Levels for Sheep?
30-50 ppm

generally no clinical signs until stressful event pushes liver to blow.
Copper Tox in Dogs?
Bedlingtons, WHighWhites, Skye Terriers

slow development of chronic active hepatitis
Treatment of Copper Tox?
Rums usually dead already....or Tx is unsuccessful

Dogs - D-penicillamine promotes urinary excretion of copper
Molybdenum

what is it needed for?
required for xanthine enzymes as well as sulfite oxidase
three way interaction with copper and sulfur
Rums more sensitive (cattle mostly, deer most rz)
What effect does a high sulfur diet have on rums?
Increase Mo absorption

Decrease Cu absorption
Molybdenum

Signs of toxicity?

Dx?
Chronic Diarrhea

Emaciation, relative Cu deficiency, CT/Bone abnormalities, Abortions

Liver - High Mo, Low Cu
Fluoride

Source?
Phosphate Supplements (which should be defluorinated)
Fluoride

Where does it go?
and what does it do?
Bone and Kidney

Fl replaces Hydroxyapatite - delaying and altering mineralization (organic oxidation = brown/black teeth)
Excessive Bone Remodeling of Long Bones
Acute Fluoride Toxicosis

Chronic Fluorosis
Excitation, Urinary/Fecal incontinence, cardiac failure, death

dry haircoat, dry skin, weight loss
Iron
most abundant trace mineral in the body
sources - supplements, fertilizers and soil
Iron Toxicosis
Direct Corrosion of GI tract --> increased presence of unbound blood Fe --> Lipid Peroxidation --> membrane damage (fatty necrosis of MYOCARDIUM), reduced CO, increased cap. permeability
Iron Excretion
There is NO NORMAL mech to eliminate Iron

So try to convert the elemental iron ingested into an iron salt (less severe form of Iron)
Level of Iron for Toxicosis?
Dogs - 20 mg/kg nontoxic, over 60 = serious signs

All animals 100-200 mg/kg is potentially lethal
Define

A. Hemochromatosis

B. Hemosiderosis
A. Pathologic tissue accumulation of Iron

B. Non-Pathologic accumulation of Iron
Four Clinical Phases of Fe Toxicosis:
Stage 1: 0-6hrs
vomit, diarrhea, GI bleed

Stage 2: 6-24hrs
transient/latent period

Stage 3: 12-96hrs
Clinical signs - CV signs, liver damage, possibly Death

Stage 4: 2-6 weeks
GI ulceration, possibly strictures
Iron Tox Diagnosis?
Serum Iron Level and TIBC (total Iron binding capacity)

if Serum Iron > TIBC, you may have severe systemic trouble
Iron Tox Treatment?
AC is NOT effective
...but Anatacids help to precipitate Fe to nonabsorbable form in GI
(NaPO4, NaHCO2, MgOH)

Supportive Care
+/- Chelation if severe (Deferoxamine)
Sodium Toxicosis
gastroenteritis, e- imbalance, severe dehydration (>10%)

Hypernatremia -- Sodium PASSIVELY enters CSF, but must be ACTIVELY pumped out --> E-deficiency, Na trapped in Brain

...now dehydrated animal is given water --> Cerebral Edema

ACUTE DEATH
Sodium Toxicosis Treatment
Replace H2O deficit SLOWLY (over several days)
~0.5% body weight in water at 1 hour intervals
Zinc

Sources
Nuts/Bolts, ZnO2 ointments, Pennies from 1983 on, Galvanized containers, pipes, etc...
Zinc

Absorbed where?
Interactions with?
Excreted?
Duodenum
Copper decreases Zn absorption and vice versa
Feces (chelated Zn in Urine)
Zinc Toxicosis
Severe Intravascular Hemolysis

samples in Royal-Blue Top tubes
(most other tubes have some Zn in their rubber)
Zinc Toxicosis Treatment?
Remove foreign bodies (endoscopy/Sx)
Supportive Care
+/- Chelation