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Toxicology > Introduction to Metals > Flashcards

Introduction to Metals Flashcards

1
Q

What functions do metals serve in biology?

A
  • Easily donate and accept electrons
  • Form water soluble cations through electron loss
  • Perform essential biological functions
    • Electron transfer
    • Redox reactions
    • Electrochemistry and signaling (Ex: Na, Ca, K)
    • Structural (Ex: Ca in bone)
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2
Q

What are the toxicity mechanisms of metals?

A
  • Oxidative damage (Zn)
  • Altered electrophysiology and osmotic states (Na)
  • Competition with normal elements for absorption (Mo/Cu)
  • Incorporation into proteins in place of normal constituents (Pb/Ca)
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3
Q

What metals are of the highest concern for veterinarians?

A
  • Lead
  • Copper
  • Zinc
  • Sodium
  • Iron
  • Arsenic
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4
Q

What is a metal?

A
  • A chemical element whose atoms readily lose electrons to form cations, and form metallic bonds between other metal atoms and ionic bonds with nonmetal atoms
  • Exist as elements or compounds
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5
Q

`What is a heavy metal?

A
  • Poorly defined subset of elements tat exhibit metallic properties
  • Relatively toxic (Pb, Sn, Hg, Tl, Au, Pt, Ba)
  • Considered meaningless by IUPAC
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6
Q

What are the toxicological properties of heavy metals?

A
  • Cumulative in biological systems
  • Can change valence
  • Complex with organic molecules
  • Persistent in the environment
  • Can be strong oxidants
  • Bind to essential molecules
  • Many metal to metal interactions
  • Clinical toxic effects vary widely
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7
Q

What are the oxidation states of heavy metals?

A
  • Multiple states
  • This lead to the formation of different compounds having different toxicological properties
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8
Q

What elements form covalent bonds with heavy metals?

A
  • Sulfur, oxygen, and nitrogen
  • Can be basis for toxicity
    *
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9
Q

What animals are commonly affected by lead poisoning?

A
  • Cattle
  • Dogs
  • Cats, Pet birds, zoo animals
  • Sporadically hoses and sheep
  • Pigs are resistant
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10
Q

What are the major effects of lead?

A
  • Nervous system is the primary target
  • Mild irritant to GI mucosa
  • Anemia due to interference with RBC maturation
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11
Q

What are the sources for lead?

A
  • Lead carbonate used to be a common component of paint
    • Strictly controlled since the 1970’s
    • Old buildings/ stored paint remain important sources
  • Lead-acid Batteries
  • Industrial/mining pollution
  • Lead shot, bullets
  • Lead weights
  • lead sinkers
  • lead toys
  • Motor oil form leaded gas engines
  • Old grease
  • Old linoleum
  • Pollution
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12
Q

What are the important kinetic factors of lead?

A
  • More surface area = more absorption
    • Lead/acid battery plates
    • GIT mucosal surface area
  • Acidic environment = more absorption
    • low pH leads to ionization
  • More time = more absorption
    • lead particles may be trapped in the reticulum
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13
Q

What is the half-life of lead in various tissues?

A
  • Blood - a few days
  • Liver/kidney - weeks
  • Brain - months
  • Bone - >1000 days (practically a lifetime burden)
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14
Q

What is the common signalment for lead poisoning?

A
  • Seasonal incidence - spring, early summer
  • Age - often younger animals (pups, calves)
  • Locations:
    • Dogs - older homes, low income areas, work places
  • Cattle - casual management, old buildings, junk piles
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15
Q

What are the Toxicokinetics of lead

A
  • Ingested lead typically requires solubilizing
    • Acidic environment of stomach vs. lead in soft tissue
    • Poorly absorbed - ~2% from GI tract
    • Dust inhalation - fine particles < 0.5 um
  • Tissue binding - first to erythrocytes
    • 90% binds to RBC, some to albumin
  • Crosses blood-brain barrier and placenta - embryo toxicity
  • Incorporation into bone:
    • storage site, detoxification mechanism
    • Lead line - in radiographs, in gums
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16
Q

How is lead eliminated from the body?

A
  • Fecal
  • Urinary
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17
Q

What are the acute toxicity amounts of lead?

(Calves, cattle, dog, horse, ducks geese)

A
  • Calves - 40-600 mg/kg
  • Cattle - 600-800 mg/kg
  • Dog - 191-1000 mg/kg
  • Horse - 500-750 mg/kg
  • Ducks - 18 pellets of #6 shot
  • Geese - 25 pellets of #6 shot
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18
Q

What are the chronic toxicity amounts of lead?

(Calves, cattle, dog, horse, ducks geese)

A
  • Calves - none (would be adults)
  • Cattle 1-7 mg/kg
  • Dog 1.8-2.6 mg/kg
  • Horse 2.4-7 mg/kg
  • Ducks 2 mg/kg
  • Geese - unknown
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19
Q

What is the MOA of lead?

A
  • Binding to sulfhydryl groups
    • Heme synthesis ⇓
    • Altered GABA transmission
  • Competition with divalent cations Ca++ ions
    • Displace Ca++ from binding proteins
    • Altered nerve and muscle transmission
  • Inhibition of membrane associated enzymes
    • Calmodulin, Na./K pumps
  • Altered vit D metabolism
    • Impaired Ca++ absorption & Zn related enzymes
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20
Q

What is the clinical presentation of lead toxicosis?

A
  • Clinical onset usually delayed several days
    • Time for absorption, binding to active sites
  • Depends on form of lead
    • Organic: rapidly absorbed and distributed
    • Metallic: slower absorption & onset
      • Carbon, nitrate, oxide salts > acetate & chloride salts
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21
Q

What are the clinical signs of lead toxicosis in most species?

A
  • Onset = several days after exposure
  • Signs quite variable: slow vs explosive
  • GI + Neurologic combo
    • Complete anorexia
    • CNS depression / Convulsion
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22
Q

What are the clinical signs of lead toxicity in Dogs?

A
  • GI: vomiting, anorexia, tender abdomen, diarrhea/constipation
    • usually appear first
  • CNS: lethargy, hysteria, convulsions, ataxia, blindness, mydriasis
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23
Q

What clinical pathology is found in dogs with lead toxicosis?

A
  • Increased nucleated RBC’s and basophilic stippling without severe anemia
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24
Q

What are the differential diagnosis for lead toxicosis in dogs?

A
  • Canine distemper
  • Parasites
  • Methylxanthines
  • Tremorgenic mycotoxins
  • NSAIDs (GI)
  • Salt toxicosis
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25
Q

What are the clinical signs of lead toxicosis in cats?

A
  • Less common due to eating habits
  • Lethargy
  • Anorexia
  • Vomiting
  • Weight loss
  • Excessive salivation
  • Neurologic signs can be minimal
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26
Q

What are the clinical pathology findings in cats with lead toxicosis?

A
  • Inconsistent nucleated RBC’s and basophilic stippling
  • Elevated AST, ALP
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27
Q

What are the differential diagnosis for cats with lead toxicosis?

A
  • Organophosphates
  • Bromethalin
  • methylxanthines
  • Hepatic encephalopathy
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28
Q

What are the clinical signs of lead toxicosis?

A
  • GI: anorexia, rumen stasis, gaunt, salivation
  • CNS: blindness, muscle twitching, head bobbing, depression, bruxism, circling, convulsions
  • Acute convulsive death in calves
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29
Q

What are the differential diagnosis for cattle with lead toxicosis?

A
  • Water deprivation
  • Polio
  • Organophosphates
  • nervous coccidiosis
  • Rabies
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30
Q

What are the clinical signs of Birds with lead toxicosis?

A
  • Depressed
  • Weak
  • Anorectic
  • weight loss
  • esophageal paralysis
  • regurgitation
  • diarrhea
  • Wing droop
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31
Q

What are the clinical signs of lead toxicosis in horses?

A
  • Recurrent laryngeal nerve paralysis results in “roaring”
  • Ataxia, incoordination
  • Foals - metaphyseal sclerosis
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32
Q

What is the gross pathology of lead toxicosis in cattle?

A
  • Lead objects in rumen or stomach
  • Rumen protozoa dead or inactive
  • Laminar cortical necrosis (DDx from PEM)
  • Inconsistent acidophilic intra-nuclear inclusions in renal tubules
  • Porphyrinuria
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33
Q

How is Lead toxicosis diagnosed?

A
  • History, clinical signs
  • Lead in whole blood
    • >0.35 ppm (0.25 avian)
    • Normal = < 0.05 ppm
  • Lead in Kidney or Liver
    • >8 ppm
    • Normal = <0.5 ppm
  • Radiography- Lead objects in gut
  • Peripheral blood smear (dogs)
    • nucleated RBC’s, basophilic stippling
  • Ca-EDTA mobilization test
  • Urinalysis: increased delta aminolaevulinic acid (ALA), Lead concentration
34
Q

What is the treatment for lead toxicosis?

(Broad sense)

A
  • Remove animal from source
  • Stop further absorption
  • Increase excretion-chelators
  • Supportive care
35
Q

How can further absorption of Lead be stopped?

A
  • Decontaminate GI tract
    • cathartics, enema according to species
  • Endoscopy or gastrotomy to remove objects
  • Oral MgSO4 in cattle (laxative and formation of insoluble PbSO4
  • Charcoal NOT effective for metals
36
Q

What Chelators are used for lead toxicosis treatment

A
  • CaEDTA - IV/SQ
    • standard for cattle - FDA restricts use
  • D penicillamine - PO in SA
  • Succimer
    • DMSA (dimercaptosiccinic acid) Chemet, Bock (PO in SA)
      • Approved (dogs) 20mg/kg TID for 5 days then BID for 2 weeks
      • Effective in cattle, dosage and expense preclude
37
Q

What is the supportive care for lead toxicosis?

A
  • Fluids, thiamine
  • Control seizures: valium, pentobarbital+/-
  • Mannitol, dexamethasone for cerebral edema
  • Antioxidants (Vit C, E): N-acetylcysteine
  • Good nursing care
38
Q

What are the public health concerns with lead?

A
  • Children in household exposed to the same lead source as pets
  • Food safety:
    • long residue time in bone
    • transfer to milk in early lactation
    • Residues can vary from weeks to months
    • Contact state veterinarian recommended
39
Q

What is Arsenic (As)?

A
  • Metalloid
  • Elementa, organic, and inorganic
  • Trivalent (+3) comes as organic and inorganic
  • Pentavalent (+5) comes as organic and inorganic
40
Q

What are the sources of Arsenic?

A
  • Mining sites and smelters
  • Insecticides and herbicides
  • Wood preservative
  • Medicinal (heartworm therapy)
  • feed supplements
41
Q

What are the sources for inorganic Arsenic?

A
  • Old pesticides - Lead arsenate, herbicides
  • Terro ant poison
  • Ashes of Chromated Copper Arsenate (CCA) lumber
    • common source for cattle
42
Q

What are the Toxicokinetics of Arsenic?

A
  • Absorption of different forms is variable
    • major toxicity factor
  • Distribution:
    • Accumulation initially in liver and then slowly distributed to other tissues (ie spleen, liver, lung) later accumulates to keratinized tissue
    • Crosses placenta and is embryotoxic
    • Crosses blood-brain barrier
    • Hair and keratinized tissue - eliminated in the feces and urine
43
Q

What are the toxic mechanisms of inorganic Arsenic?

A
  • Binds with sulfhydryl enzymes
  • Blocks cellular respiration
    • Acts on tissues with high respiration
      • Gut epithelium, capillaries
  • Phosphate competition - uncouples oxidativephosphorylation
  • Toxicity: trivalent is 5-10x more toxic than pentavalent
    • Arsenite (+3) > Arsenate (+5) > organic As
  • Arsenite- inhibits ATP synthesis
    • sulfhydryl inhibition (enzymes)
    • a-lipoic acid - TCA cycle
  • Arsenate- resembles Pi in structure and reactivity, replaces phosphate
44
Q

What Arsenic was used in Heartworm therapy and what are the effects?

A
  • Thiacetarsamide - Caparsolate
    • Vomiting
    • Liver and kidney damage
  • Ivermectin, melarsomine (melaminylthioarsenate) and Diroban (melarsomine HCL) commonly used now
45
Q

What are the GIT clinical signs of inorganic Arsenic toxicosis?

A
  • Vomiting
  • Intense abdominal pain
  • Diarrhea (+/- blood)
  • Fluid loss
  • Maybe acute death (hours)
  • Marked dehydration
  • Weakness, staggering gait
46
Q

What lesions are common with inorganic arsenic toxicosis?

A
  • GI hemorrhage, edema, fluid filled
  • Sloughing, mucosa
  • Renal tubular degeneration
47
Q

How is inorganic arsenic toxicosis diagnosed?

A
  • Arsenic analysis of kidney, liver >8ppm
  • Suspect material
  • Urine contains As if kidneys are functioning
  • Accumulates in hair for chronic exposure
  • Blood is NOT a good diagnostic source
48
Q

What are the treatment options for inorganic arsenic toxicosis?

A
  • Most attempts are futile
  • Rehydration
  • BAL (dimercaprol) is classic antidote, best before signs
  • Thiotic acid 50mg/kg q8hr
  • Succimer (DMSA)
49
Q

What is Iron (Fe)?

A
  • Common in human dietary supplements and vitamin/mineral tablets
  • Ingestion of concentrated Fe sources can be toxic to children and pets
  • Injections can be toxic
50
Q

What are the levels of toxicity of Iron?

A
  • Non toxic <20 mg/kg
  • Mild-Moderate 20-60 mg/kg
  • Serious >60 mg/kg
  • Life threatening >200 mg/kg
51
Q

What are the 4 stages of clinical effects of Iron toxicosis

A
  1. 0-6hr: Corrosive effects
    1. nausea, vomiting, diarrhea, GI hemorrhage
  2. 6-12hr: Apparent remission
  3. 12-24 hr (in severely poisoned dogs)
    1. Severe lethargy
    2. Reocurrance of GI signs
    3. Metabolic acidosis
    4. Liver necrosis
    5. Coagulopathy
    6. Cardiovascular collapse, shock
  4. Several weeks later:
    1. scarring and stricture of GI tract
52
Q

How is Iron toxicosis diagnosed?

A
  • History, Clinical signs
  • Abdominal radiograph
    • mass of pills in stomach
  • Serum Fe:
    • normal 80-249 ug/dL
    • 300-500 ug/dL monitor
    • >500 chelation therapy
    • If serum Fe>TIBC = poison likely
      • (Total iron binding capacity)
53
Q

What is the treatment for iron toxicosis?

A
  • Emetic in alert animal, gastric lavage or gastrotomy
    • NOT CHARCOAL
  • Fluids, electrolytes, A/B balance
  • GI protectants
  • Chelation therapy:
    • Deferoxamine (Desferol)
    • Initial IV infusion - 15 mg/kg/hr
    • IM 40 mg/kg q 4-8hr
    • Continue until serum Fe is below 350 ug/dL
54
Q

What is Mercury (Hg)?

A
  • Toxicosis is infrequent and sporadic
    • in last 30 years are associated with Hg fungicide treated seed
  • Unusual metal because it is a liquid at normal temperatures
  • Hg vapor poses a substantial hazard
  • 3 different forms in the environment
    • Elemental Hg, Hg0- metallic or vapor
    • Inorganic mercury, Hg Salts HgCl2
    • Organomercurial compounds,
      • alkyl forms = ethyl, methyl, propyl, dimethyl, etc, and aryl forms of Hg such as phenylmercuric acetate
  • Hg accumulates as alkyl, methyl, and ethyl mercury
55
Q

What are the sources for Mercury?

A
  • Batteries
  • Some pharmaceuticals -
    • calomel - antiseptic salve, in laboratory electrodes and as a fungicide
  • Industrial effluents, sewage sludge
  • Ocean waters - marine fish, shell fish, mackerel, shark, swordfish, tilefish, tuna
  • Thermometers, barometers fluorescent tube
56
Q

What are the toxic levels of Mercury?

A
  • Elemental Hg is low in toxicity orally
  • Hg salts: 1mg/kg/day is toxic to cats in 15 days
  • Hg salts: large animals 8-12 mg/kg
  • Methyl (alkyl) mercury 0.2 - 0.5 mg/kg
  • Phenyl (aryl) mercury - Swine 1 mg/kg
  • Highly toxic on a chronic basis
57
Q

What are the clinical effects of inorganic mercury?

A
  • Gi and renal tubular necrosis
58
Q

What are the clinical effects of organic mercury?

A
  • Crosses BBB and Placenta
  • Neurologic fibrinoid degeneration of arterioles
  • neuronal necrosis ⇢ blindness, staggering, incoordination, recumbency, death
59
Q

How is mercury absorbed?

A
  • Elemental Hg poor GIT absorption
    • Vapors are absorbed and dangerous
  • Salts and organ mercurial are absorbed in the GIT
60
Q

How is Mercury excreted?

A
  • Kidney ⇢ urine
  • Fecal
  • Lungs
61
Q

What are the mechanisms of toxicity of Mercury?

A
  • Primary targets are the kidneys and CNS
  • Bind to sulfhydryl groups
  • Inhibit enzymes and protein synthesis
  • Inhibit mitochondrial function by binding to alpha lipoic acid and thioctic acid
  • Sulfur containing organic acid cofactor involved in aerobic metabolism
  • Pyruvate dehydrogenase complex (PDC)
62
Q

How is Mercury toxicosis diagnosed?

A
  • Whole blood > 1ppm
  • Liver
  • Kidney
  • Hair
  • Urine
  • Feeds
63
Q

How is Mercury toxicosis treated?

A
  • Acute exposure:
    • Egg white, activated charcoal, sodium thiosulfate (0-1 g/kg)
  • Saline cathartic or sorbitol
  • Oral penicillamine (1-50mg/kg) orally
  • DMSA
  • Chronic organic exposure: selenium and Vit E
64
Q

What risk does mercury pose to public health?

A
  • Bioaccumulation & bio magnification in the food chain
    • sediments ⇢ fish ⇢ mammals
  • Mercury residues in kidney & muscle tissue
    • highest concern in fish - (0.7 - 1.5 ppm)
65
Q

What is Thallium (Tl)?

A
  • Discovered in 1861 Sir William Crooks
  • Elementary Tl is Non-toxic
  • Monovalent and trivalent salts are very toxic
    • Thallous - +1 oxidation state
    • Thallic - +3 oxidation state
  • Heavy metal - very toxic and highly cumulative
66
Q

Sources of thallium?

A
  • World production is 12 tons/yr
  • Semiconductors, photocells, optic glass, thermometers
  • Tl201 radioactive tracer used in heart scintigraphy to detect myocardial ischemia
  • Rodenticides
67
Q

What is the MOA of Thallium?

A
  • Blocks energy utilization by Na-K-ATPase channel
    • blocks active transport of K across the cell membrane
      • Similarities in charge between K+ and Tl
      • Tl has a 10x greater affinity than K+ in neuronal, cardiac, and skeletal muscle cells
      • Half-life of 30 days
  • Blocks energy production from glucose
    • ADP to ATP by pyruvate kinase - K requiring enzyme
      • Tl binds with 50x affinity compared to K+
  • Damages riboflavin, forming an insoluble complex and intracellular sequestration of vit B6
  • Binds to SH groups and interferes with formation of disulphide bonds in keratin, structural damage to hair and nails (depilatory)
  • Causes activation or inhibition of other enzymes
    • ALA synthetase, B12 metabolism
68
Q

What are the clinical effects of thallium toxicosis?

A
  • Multisystemic disease
    • GI necrosis - sever hemorrhagic gastritis, congested oral mucosa
    • Neurologic - trembling, motor paralysis, mental retardation
    • Alopecia and skin sloughing from 7 days to 2-3 weeks after ingestion, renal and liver injury
    • Blindness
69
Q

How is Thallium toxicosis diagnosed?

A
  • Urine thallium (any concentration is significant)
  • Kidney
  • liver, feces
70
Q

What is the treatment for Thallium toxicosis?

A
  • Radiogardase - prussian blue insoluble capsules
    • ineffective once clinical signs are apparent
  • Dithizon - chelator for Thallium
71
Q

What is Fluoride?

A
  • Reactive, water soluble non-metal
  • Common in nature, variable in distribution
72
Q

What are the sources for fluoride?

A
  • Mining deposits
  • Rock phosphates (feeds)
  • Water from deep wells/geothermal water
  • Industrial pollution (particles may settle on pastures)
  • Production of industrial processing of aluminum ores or phosphate fertilizers
    • fertilizers and calcium phosphate minerals must be defluorinated
  • Pesticides
73
Q

What are the _______

A
  • Affects mineralized tissue
    • teeth bone
  • Deposits in hydroxyapatite crystal of bone and distorts normal Haversian system remodeling
  • Dental fluorosis is dystrophic formation of dentin and enamel in erupting teeth only (marker for time of exposure)
74
Q

What are the clinical effects of fluoride toxicosis?

A
  • Chronic exposure:
    • Progressive debilitating disease
    • Cattle, horses, wild herbivores
  • Osteofluorosis:
    • Bone formation on outside of long bones (exostoses)
      • produces lameness
  • Dental fluorosis:
    • Softening of tooth enamel, early wear
75
Q

What are the kinetics of fluoride?

A
  • Rapidly absorbed
  • Excreted through urine
    • some through milk
  • ~50% absorbed dose sequesters in bone
    • Mostly in developing/remodeling bone
    • Developing teeth - erupted teeth unaffected
76
Q

What is the clinical picture of Fluoride toxicosis?

A
  • Large, acute exposure:
    • GI irritation and kidney damage
  • Moderate/Chronic exposure:
    • more common
    • affects bones and developing teeth
      • Osteogenesis is interrupted/altered
      • Prominent effects seen in long bones, mandibles and rib surfaces
        • Articular surfaces are NOT affected
      • Spurring around joints produce pain and lameness
        • Abnormal postures, stiffness, disinclination to move, weight loss
77
Q

How is Fluoride Toxicosis diagnosed?

A
  • History, clinical signs, lesions
  • Feed, mineral, and water analyses
  • Biopsies of coccygeal vertebrae or ribs
  • Urine fluoride may be helpful within 1-3 weeks of exposure
    • kidney and liver can be tested postmortem
78
Q

What are the clinical signs of fluoride toxicosis?

A
  • Lameness
  • weight loss
  • elongated hooves
  • lapping water
79
Q

What are the common lesions seen with fluoride toxicosis?

A
  • Dental fluorosis in erupting teeth
  • Exostosis of limbs, ribs, mandible
  • Fl analysis:
    • Urine (15-20 ppm) - recent
    • bone (>3000 ppm) - prolonged exposure
80
Q

What is the treatment for Fluoride toxicosis?

A
  • No specific treatment
    • poor prognosis
    • Pain management and soft feed may allow salvage following extended recovery periods
  • Avoid exposure
  • Aluminum or Ca-carbonate at 1% of diet will reduce fluoride absorption

Toxicology (25 decks)

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