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Toxicology ME I
Question | Answer |
---|---|
uses of arsenicals | insecticides, medicinals, wood preservatives, hematinics; phenylarsonic - feed additive (growth stim) poultry/swine |
dz syndrome: inorganic arsenical | GIT, capillaries |
dz syndrome: organic trivalent arsenical | GIT, capillaries |
dz syndrome: pentavalent organic arsenical | neurological syndrome |
Tx; 2 most important intoxications | 1 lead, 2 arsenic |
arsenics are __________ | persistant (once there, always there) |
Fowler's solution: use? chemical name (ingredients)? | tonic, conditioner; potassium arsenite |
phenylarsonic compounds: use | feed additives - poultry/swine; growth stimulant (inc feed efficiency); tx swine dysentery |
withdrawal pd assoc w/phenylarsonic compounds | 5 days |
list 2 arsenic-derived feed additives | arsanilic acid & sodium salts; roxarson |
arsenate: MoA | uncouple oxidative phosphorylation |
arsenite: MoA | react w/sulfhydryl groups of proteins-> inhib enzymes by blocking active groups (alpha-keto oxidases [contain dithiol gorups; oxidate pyruvate], lipoid acid [coenzyme for pyruvic acid oxidase & alpha-oxyglutaric acid oxidase]) |
importance of BAL in regards to arsenic | reverses arsenite inhibition of lipoic acid (essential coenzyme for pyruvic acid oxidase & alpha-oxyglutaric acid oxidase) |
arsenic induces __________ & ____________ | vasodilation & capillary damage |
arsenic organic pentavalent: MoA? | may interfere with vit B6 & B1 -> inhib myelin formation -> neuro dz |
how does an animal develop a tolerance to arsenicals? | low doses over a long period |
absorption of inorganic arsenic depends on _______- | solubility |
arsenic: absorption? | primarily GIT; minimally through intact skin |
arsenic: pentavalents or trivalents are better absorbed? | pentavalents |
arsenic: dist in tissues | accum in liver; slow dist to other tissues; will cross placenta; chronic - stored in bones, skin, keratinized tissues |
arsenic: redox equilibria favors what? | oxidation (+3 form) |
arsenical excretion | urine, feces, sweat, milk; trivalents - slow in feces; pentavalent - fast in urine |
arsenical: relative toxicity | trivalent inorganic (As+3/arsenite) > pentavalent inorganic > tri org > pent org; most metals - org > inorg |
arsenicals: which forms are the most toxic | more finely ground; solutions (dips, defoliants) |
arsenicals: causes of poisoning | therapeutic agents in debilitated animals; not biodegradable; human carelessness & ignorance |
arsenical: clinical signs | GI (abdominal pain, hemorrhagic diarrhea, salivation), CNS (grinding teeth, weak, incoordinated, rear limb paralysis, convulsions, prostration), hematuria, brick red mm, enlarged joints, unthrifty |
phenylarsonic clinical signs | most seen in pigs, may see in poultry; neuro - incoordinated, drunken hog syndrome, posterior paralysis; blindness, skin erythema; signs reversible unless progressed to nerve damage |
arsenical: lesions | may have none; GI irritation - hemorrhage, fluid in GI lumen, hyperemia of abomasum; indicative of capillary damage; soft, yellow liver |
arsenical: lesions are indicative of __________ | capillary damage |
phenylarsonic: lesions | downer pigs may have severe abrasions along w/muscle atrophy; subacute toxicosis in swine = pale yellow liver; demyelination (optic n, posterior cord) |
arsenic: early Tx | bind arsenic! emetics, gastric lavage, milk, egg white, sodium thiosulfate, saline purgative; success less likely in LA |
arsenic: late Tx (>4 hrs) | dimercaprol (BAL), sodium thiosulfate, supportive measures |
phenylarsonic compounds: tx | no effective Tx |
arsenic: where do you look for levels? | liver, kidney; urine, fecal; keratinized tissue; should NOT be foudn in phenylarsonic intox |
arsine (AH3): importance | one of most toxic arsenicals; acids + arsenic-containing metals + heat; industrial prb |
arsine: clinical signs | humans: GI, intravasc hemolysis, disturbance of vasc bed (pulm edema, cyanosis), ECG abnormalities, hemoglobinuria, liver dysfctn, delirium, coma, death |
arsine: tx | none good; BAL for chronic intox |
tissues for qualitative tests for arsenic | stomach contents, tissue, urine, feces |
qualitative tests for arsenic (2) | reinsch, gutzeit |
reinsch test: principle | Arsenic is precipitated from HCl solutions as gray copper arsenide |
gutzeit test: principle | Reaction of arsine gas w/concentrated aquious solution of silver nitrate Yellow color consisting of silver arsenide & silver nitrate forms in an aquious sooution -> turns black due to separation of metallic silver |
quantitative test for arsenic | atomic absorption spectroscopy |
lead: sources | paint, lead storage batteries, vegetation sprayed w/lead arsenate, White Lotion (lead acetate in medications), residue from exhaused fumes from leaded gasoline on forages, ing of lead shot, boiled linseed oil used for cathartic (old), smelters, gasoline |
lead: abs | GI primarily (young>adult); skin: alkyl-Pb compounds (lipid-sol, crosses BBB); resp - minor |
lead is __________ | cumulative; repeated small doses may prove toxic |
lead: systems affected | nervous, GI, renal, BM/blood |
lead: distribution | bound to RBC; initial deposit in soft tissues (renal cortex*, liver); redist to bone, teeth, hair (95% in bone) |
lead: biotrans | inorganic - none; alkyl lead, tetraethyl lead, tetramethyl lead -> dealkylated - tri-alkyl compounds (v toxic, biotrans to inorganic lead) |
lead: excretion | human adult - urine; infants/lab animals - fecal (biliary); domestic animals: fecal (biliary): feces (oral exposure), bile (abs); urine minor, milk in proportion to [] in RBC; clearance takes weeks |
lead: clinical signs (systems) | gastroenteritis, neuro damage, erythrocytic, renal; death |
lead: clinical signs (acute) | death; GI - anorexia, salivation, vomit, diarrhea, colic, abd pain; CNS - depression, m weakness, prostration, blindness, tetany, convulsions, coma; circling/head pressing (cow); viscious, clamping jaws, froth @ mouth (dogs); paralysis/knuckling (horses) |
lead: clinical signs (chronic) | sudden development of acute syndromes; + weakened <3/resp actions, ventral edema; horses - roaring, aspiration pneumonia |
lead: pathogenesis | interfere with SH groups on enzymes; major systems affected: CNS, PNS, kidney, blood, hematopoeitic; GI |
lead: toxicity | repeated small doses cause toxicity; illnesses can mobilize lead deposits -> acute lead poisoning; lower doses required in young |
lead: post mortem lesions - acute poisoning (cattle) | immediate necropsy - no lesions; delayed - odor, skel m is dirty, red-gray; gastroenteritis + hemorrhages; pale liver, lobular degen; congested kidneys, intranuc incl bodies; <3 - petechiation, ecchymosis; brain/spinal cord - CSF accum; lungs - congested |
lead: post mortem lesions - chronic (horses, dogs, sheep) | anemia (chonic hemolytic, hypochrom), basophilic stippling; lead line on gingival mucosa; laryngeal paralysis (eq); liver yellow, degen; kidney degen, fibrotic, tubular damage, intranuc incl bodies; brain - vasc endoth swelling, necr vasc change |
lead: Dx | circumstantial; clinical/post mortem; radiography, lab hemogram, chemical detection |
lead: radiography | lead line: metaphysis of long bones - radiopaque bands above open epiphyses of distal radius, ulna, metacarpals (immature dogs poisoned 10d+); shots/bullets/lead-containing obj |
lead: hemogram | neutrophilic leucocytosis w/left shift; PVC normal; hypochromic anemia (chronic Pb); nRBC, basophilic stippling, immature RBC; BM - inc erythroid activity |
lead: what sampls? | blood, feces, liver, *kidney cortex |
lead: chemical detection in blood/feces & timeline | elevated blood & feces = exposure w/in 2-4 wks; just blood elevated = > 4 wks ago |
lead: primary aim of Tx | immobilize Pb |
lead: Tx | remove from GIT (purgative, emetic, gastric lavage); chemical antidote (succimer, soluble sulfates, CaNa2EDTA, BAL if severe neuro signs); sedatives, thiamine |
lead: EDTA caution | Pb is removed from storage sites in body more rapidly than EDTA can chelate it -> acute signs in chronically exposed animals => in chronic cases, dec dosage of EDTA |
copper/molybdenum: how are they related? | toxicity of one = a deficiency of the other (with adequate sulfate (SO4)) |
copper toxicosis occurs primarily in? | sheep; bedlington terriers - congenital prb w/copper accum; wilson's dz in humans; sheed fed cattle feed - 4H & FFA lambs |
molybdenum toxicosis occurs primarily in? | catle, young; may also occur in young lambs (Swayback = neuro dz - myelin not laid down properly, loss of wool) |
copper/molybdenum: idea ratio | Cu:Mo 6:1 |
copper toxicosis | typical heavy metal signs + intravasc hemolysis; usually chonic accum in liver due to diet, stress -> released -> hemolysis, hepatic necrosis -> kidney injury |
copper toxicosis: usual sign | sudden hemolytic crisis -> anemia, jaundice |
copper toxicosis lesions | icterus, gun metal kidneys, yellow-friable liver, black-berry jam spleen, hemoglobinuria |
copper toxicosis: Tx | remove source of copper, blood transfusions, penicillamine, trientine, s-adenosyl methionine (methyl donor for liver), ammonium tetrathiomolybdate, ammonium molybdate, zinc (prevent hemolytic crisis), molybdenized licks |
molybdenum toxicosis: typical presentation | chornic dz; poor doers, chronic diar, hypoproteinemic, achromotrichia (change in color, lose skin pigment), poor repro performance, anemia, jt prbs; look like they're heavily parasitized; sheep may have wool prbs, labs w/neuro prbs (Swayback) |
where is molybdenum toxicosis usually seen? | mining, industrial; molybdenum fertilizers |
molybdenum toxicosis: treatment | copper glycinate, change diet |
copper/molybdenum: in non-ruminants | interactions not as marked; Cu tox dec by Fe, Zn; molybdenum may be necessary for xanthine oxidase & antagonized by tungstate |
copper toxicosis in non-ruminants | no hemolytic crisis; jaundice (pigs); liver, kidney degen; treat w/penicillamine |
molybdenum toxicosis in non-ruminants | anemia; bone deformation/decalcification; cerebral edema/necrosis; achromotrichia; fetal resporptoin; aortic rupture; reduced ceruloplastin |
mercury: sources | electrical equip, switches, manufacture of chlorine & NaOH, antifouling paints, catalysts, amalgam, antifungals, antiseptics, thermometers; eye ointment, antifungal |
elemetal mercury (Hg0): abs | vapor - lungs, skin (v toxic); solid-liquid - almost non-toxic; no charge = v lipid soluble; poorly abs from GIT |
elemetal mercury (Hg0): biotrans | may be oxidized to inorganic mercury in blood, or may be carried by blood to brain where it is oxidized |
elemetal mercury (Hg0): distribution | accum in kidneys |
alkyl mercury (methyl & ethyl mercury): abs | highly lipid sol |
alkyl mercury (methyl & ethyl mercury): distribution | throughout the body |
alkyl mercury (methyl & ethyl mercury): biotrans | dealkylated & converted to Hg+2 (mercuric, inorganic); those molecules that enter CNS are delkylated & get trapped in brain bcz of loss of lipid solubility |
mercuric salts (HgCl2, Hg2Cl2) & aryl molecules: abs | mercuric chloride = rapidly abs from gut; precipitates protein on contact; mercurous cloride = insoluble, poorly absorbed & relatively non-toxic |
HgCl2: distribution | via RBC to liver & kidneys |
aryl mercurials: abs & biotrans | well-abs; mercury is removed & functions as mercuric form |
elemental solid/liquid mercury: pathogenesis, dz/organs affected, therapy | oral exposure, not readily abs; of no toxicological consequence = no therapy |
elemental vaopr mercury: pathogenesis, dz/organs affected, therapy | inhalation, lipid sol -> Hg2+ in blood = renal, some crosses BBB before exidation = CNS - neuronyl degen; primarily CNS tox, some renal; tx BAL for renal, nothing for CNS |
mercuric (Hg2+): pathogenesis, dz/organs affected, therapy | ing, GI irritation, renal tox (min CNS); GI, renal affected; Tx w/BAL |
mercurous (Hg+): pathogenesis, dz/organs affected, therapy | ingestion = GI irritation, min renal tox; tx w/BAL if necessary |
alkyl Hg++(CH3)2: pathogenesis, dz/organs affected, therapy | ing, lipid sol - dealkylated - in blood=renal tox, in CNS=neuro dz (not ionized = penetrate BBB); CNS, some renal dz; tx BAL for renal, nothing for CNS |
aryl Hg++: pathogenesis, dz/organs affected, therapy | ing, lipid sol; dearylated = doesn't enter CNS -> GI irritation, renal dz; tx w/BAL |
mercury: excretion | primarily in urine; also saliva, feces, hair; capillary damage @ sites of excretion w/hemorrhage |
mercury: toxicity | major target organ is kidney; elemental & alkyl mercury compounds also hit CNS |
mercury: MoA | will combine w/SH groups & inhibit enzymes |
mercury: clinical signs from mercuric chloride (acute) | corrosive poisoning - gastroenteritis, bloody diarr, death from shock, oral gavity is ashen-gray; acute nephritis, early diuresis w/albimunuria, anuria; precipitates proteins & affects -SH groups; arrhythmias, fibrillation |
mercury: clinical signs (chronic) | hemorrhages, hematuria, epistaxis, bloody feces; renal & GI effects; humans: salivation, swollen gums, loosened teeth, necrosis of jaw bones (mercurial ptyalism), fatigue, insomnia, motor/mental disturbances |
mercury vapors: clinical signs | psychic & emotional disturbances, motor disturbances, GI, renal, lungs |
alkyl mercurials: clinical signs | mental disturbances, ataxia, gait disturbances, incoordination, paddling, posterior paralysis, blindness, mental def; latenet pd; prenatal tox; from treated seeds & contaminated fish (japan) |
mercury: lesions | acute inorganic: gastroenteritis, acute parenchymatous nephritis, stomatitis; alkyl - may not be gross change, neuronal degen in cerebral cortex & cell loss in cerebellum, degen in cord & periph nn, prox tubule effects |
mercury: Dx (incl tissues to test) | chemical detection in tissues (kidney, liver, brain) |
mercury: Tx | protein (egg white, milk), empty stomach, cathartic; ineffective after 10-15 min; BAL (will only remove inorganic Hg, won't reverse CNS damage); penicillamine (chronic intox) |
mercury: prognosis in acute cases | absorption is rapid; chances of survival are determined in first few min |
list essential elements | fluoride, iron, cobalt, magnesium; trivalent chromium (prb) |
fluoride: sources | forages subjected to airborned contamination from industry; drinking water; feed/mineral supplements; vegetation grown on high fluoride soils |
fluoride: factors governing toxicity | level in diet; duration of exposure; type/solubility; age of animal; level of nutrition; stress; indiv biologic response |
what happens with prolonged ingestion of fluoride | accumulates in body -> chronic toxicity |
fluroide: MoA | ameloblastic & odontoblastic damage; faulty calcification of teeth; osteoblastic damage; dental, bone lesions |
fluoride: clinical signs (acute) | GI irritation & neuro signs; typical acute heavy metal signs |
fluoride: clinical signs (chronic) | debilitating dz; affects bone, teeth; dental lesions (brown, mottled teeth; excessvie wearing/crumbling); bone: hyperostosis, enlargement/roughening, first seen on metatarsals, then mandible, metacarpals, ribs; pain when encroachment on joints (ankelosis) |
fluroide: economic loss? | painful = don't move, lose wt, starve |
fluroide: diagnosis | bone lesions, urine/bone levels, feed/water levels |
fluoride: Tx | symptomatic; some aluminum salts are thought to increase excretion; prevention is best - otherwise unrewarding |
fluoride: prophylaxis | if water is high in fluoride, forage must be low; dilute feed stuffs; defluorinated rock phosphate for minerate supplements |
iron: excretion | no means of excretion |
iron: sources | injectable iron preparations, oral preparations |
iron: toxicity | overzealous use of iron preparations |
iron: MoA | high oral doses injure gut wall = inc abs; high body load = <3vasc collapse, inc cap perm, dec plasma vol; excessive liver Fe = inactivates oxidative enzymes = hepatic necrosis; metabolic acidosis; profound shock; inc serum Fe interferes w/clotting mech |
iron: clinical signs | shock, CV collapse, vomit, edema, anaphylactic-like syndrome, death; depression, liver dysfctn; hemosiderosis: liver, BM, heart dz |
iron: lesions | yellow-brown discoloration of all tissues; periportal necrosis of liver; renal damage; gastric ulceration (if oral) |
iron: Tx | symptomatic, plasma expanders (inc volume), MgO, deferoxamine (may cause hypotension) (chelating agent) |
iron: Dx | difficult |
cadmium: source | byproduct of Cu, Pb, Zn, used as allow for rust-proofing; vessels for holding food; galvanized materials; smelting effluents; NiCad batteries |
cadium: toxicity | young>old |
cadmium: where is it stored in body | 50% in liver & kidney; stored as metallotionine - high molecular wt proteins => nephrotoxic in high quantities; 90% of circ Cd in RBC, Hb, metallothionine, high molecular weight proteins |
cadmium: abs | low GI abs |
cadmium: MoA | inhibits - SH containing enzymes; may inhibit antitrypsin - pulm edema |
cadmium: excretion | humans: urine; animals: feces (bile) |
cadmium: clinical signs (acute) | oral = vomiting; inhalation of fumes (fume fever) = pulmonary edema, resp prbs, CNS disturbances |
cadmium: clinical sings (chronic) | hyperchromic anemia; BM hyperplasia; studnet growth, skel deformities; hypertension; <3 hypertrophy; chronic pulm fibrosis; chronic kidney prbs; teratogenic - rats; yellow teeth; chronic pain ("Itah itah"); carcinogenic? |
cadmium: Tx | chelating agents will INC tissue damage, esp BAL-Cd (renal damage); Vit D & Ca supp; calcium disodium EDTA may be beneficial (CaNa2EDTA) |
cobalt: pathogenesis | foaming agent in some beers in midwest & canada -> cardiomyopathy (beer drinkers cardiomyopathy); BM stimulant: inc RBC ct by 10-20% |
chromium: use | CHO metabolism (trivalent) |
chromium: toxicity & clinical signs | hexavalent = nephritis, pulm congestion, dermatitis; lung cancer, chonic ulcers in nasal septum, chronic enteropathy |
barium: source | rodenticide; barium carbonate is sometimes mistakenly used for barium sulfate |
barium: MoA | stimulates all muscle (skel, cardiac, smooth) |
barium: Tx | prevent absorption: sodium sulfate laxative -> barium sulfate (insoluble) |
magnesium: source | common feedstuffs, concentrates; supplements w/MgO are most common; toxicosis is due to excess supplementation |
magnesium: clinical signs | purgation, CNS depression, curare-like action on myo-neural junction (inhib), death from resp depression; diarrhea, dec growth, skel abnormalities, upset of Ca/P homeostasis in chicks; anorexia/diar, milk-fever-like synd in sheep |
magnesium: Tx | Ca2+ |
iodine: Source | seaweed, chilean caliche rock |
iodine: medical uses | KI & NaI treat actinobacillosis (lumpy jaw); ethylene diamine dihydroiodide (EDDI) - feed addititve (footrot in cattle, expectorant in swine/poultry, antiseptic in cattle) |
iodine tox: clinical signs | inc resp tract secretions; cough; sloughing of superficial epidermis & mild alopecia; lacrimation; cessation of egg productions (chicken); resembles Vit A def; mortality = low; may mimic hyperthyroid; infertility, abortion, dec appetite |
iodine tox: lesions | scaly skin on dorsum, around eyes; seromucous accum in URT; disruption of tracheal mucosa w/necrotic areas, squamous metaplasia & loss of tracheal cilia, neutrophilic/lymphocytic infiltratinos in lamina prop of trachea; thyroid enlargement; larynx edema |
iodine: Dx | Hx, clinical signs; elevated serium iodine; depressed immune function, interference w/titer maintenance to some Ag's |
iodine: Tx | remove from soure, animals will improve |
silver: use | astringent, disinfectant, caustic |
silver nitrate: pathogenesis | ing = gastroenteritis - denatures protein |
silver nitrate: Tx | oral NaCl: converts soluble nitrate to insoluble AgCl -> follow with demulcents |
argyria: define | chronic silver toxicity |
argyria: cuase | industrial use of colloidal silver compounds |
argyria: lesion | slate-black disocloration of skin due to deposition of silver (blue man of circus); common in japan |
selenium: source? | alkaline, well-aerated soils (ie those in high dry plains) have higher oxidation states, selenites, selenates (SeO3, SeO4); taken up by plants (obligatq, facultative, non-accum); feed additive; inj/oral |
cultivated crops, grasses, and grains: do they take up selenium? | non-accumulators; still take up some |
what is the purpose of inj/oral Se preparations? | prevention/Tx of Se deficiencies: nutritional myopathy (white m dz) (cattle/sheep); hepatic necrosis, arterioloar degen & <3 myopathy (pig); exudative diathesis, encephalomalacia & myopathy (poultry); reduce incidence of retained placenta (cow) |
selenium: MoA | normally - component o fglutathione peroxidase (prevents damage to cell membranes); assoc w/dec tissue ascorbic acid, glutathione & possible niacinamide; high doses have effects on GI mucosa & blood vessels |
selenium: toxicity | most common in grazing animals; rarely a prb in feed mixing errors for complete feeds; parenteral Se products can be v toxic, esp to young animals |
Se: clinical signs (acute) | pig: emesis, diar (like arsenic tox), weak, fever, colic, depression, dyspnea, prostration, resp failure; calve: depression, inappetance, prostration, dyspnea, death; lamb: dyspnea, convulsion |
Se: clinical signs (chornic) | blind staggers, alkali dz; hair loss, deformation/sloughing of hooves; loss of vitality, anemia, stiff gait, lame, rough hair coat, alopecia of mane/tail, separation of hoof from coronary band; paralysis in swine |
se tox (chronic): describe clinical signs in swine | paralytic form: posterior paralysis to tetraplegia; in sternal recumbancy - alert; painful coronary band lesions; porcine focal symmetrical poliomyelomalacia |
selenium tox: lesions (acute) | hemorrhagic gastroenteritis, swelling/congestion of kidney & liver, degeneration, focal necrosis |
selenium tox: lesions (chornic) | emaciation, hoof/hair loss, neuronal degen & necrosis in cerebral & cerebellar cortices; swine: focal symmetrical poliomyelomalacia; articular erosions, deformed hooves |
selenium tox: lesions (peracute) | injectible preparations: pulm edema, pleural effusion, degen of liver/kidney; lambs, pigs, calves |
selenium tox: Dx | Hx, lesions; chem analysis of feed & tissue |
selenium tox: DDx | freezing of extremities, ergotism, fluoride poisoning, laminitis due to founder, NaCl in pigs, arsenic poisoning |
selenium: Tx | of little value in acute/chronic intox; symptomatic Tx for shock; arsanilic acid may aid in biliary excretion in pigs/calves |
sulfur: uses/sources | insecticide, fungicide, purgative, tonic; in highly alkaline waters in the west; hydrogen sulfide gas is found in petroleum industry, tanneries, mines, bacterial action on sewage effluents |
sulfur: MoA | purgative & local irritant; H2S is resp tract irritant, may paralyze olfaction & medullary resp centers, paralyzes cytochrome oxidase system (similar location as cyanide); purging/diarrhea due to osmotic catharsis |
sulfur: tox | elemental: non-toxic; H2S (hydrogen sulfide): as toxic as cyanide; sources of greatest hazard to livestock - liquid manure holding pits -> collapse due to resp paralysis when pits are agitated; high sulfate in water -> polioencephalopathy in cattle |
sulfur: clinical signs | elemental sulfer: purgation, colic, depresison, muddy mm; osmotic cathartics = dehydration, shock; H2S: paralyzed olfaction, irritant to eyes & mm of resp tract, hyperpnea, loss of consciousness, resp paralysis, semicomatose; polioencephalomalacia |
what gas is responsible for the most deaths in closed animal facilities | hydrogen sulfide (excluding carbon monoxide) |
pathogenesis of polioencephalomalacia in cattle in regards to sulfur | sulfates -> rumen -> forms H2S |
elemental sulfur: lesions | inflammatory gastroenteritis w/congestion of liver & kidneys; excess gas & H2S odor from GIT |
H2S: lesions | cyanosis, pulm edema, congestion, emphysema (or no gross lesions) |
sufur tox: Dx | Hx, clinical signs, post mortem findings |
sulfur: Tx | none; TLC |
sulfur tox: prevention | can be removed from water with ion-exchange resins (expensive); remove animals from enclosed housing prior to pumping sewage lagoons |
sulfites: use | food additives for human consumption; antioxidants |
sulfites: toxicity | some humans are hypersenstiive to sulfites & can develop asthmatic attack; otherwise not toxic |
zinc: sources | galvanized containers (esp under acidic conditions); nuts, bolts, pennies (ing); industrial pollution - contaminate forage; admin of Zn in diet |
zinc: tox | relatively nontoxic; high diet in horses = anemia, arthritic/metaphyseal prbs, added copper will help (will cause hypocurprosis or copper def) |
zinc: clinical signs (acute) | GI distress, emesis, dec feed consumption, pica, reduced grwoth, heinz body hemolytic anemia, poor bone mineralization, damage to pancreas, arthritis, white m dz, nonviable newborns |
zinc: clinical signs in young puppies ing bolts, etc | vomiting, icterus from hemolytic anemia, signs assoc w/prox renal tubular necrosis - oliguria, isothenuria, oral ulcers; syncope |
zinc: lesions in canines | hemorrhagic liver & kidneys |
zinc: chronic poisoning in young horses | lesions at growth plates - jt enlargement; epiphyses become enlarged; lameness; reluctant to rise; stiff gait, incl spinal mvmts; any growth plate can be involved; inc jt fluid; Tx w/EDTA & inc calcium in diet; may cause copper def |
zinc: tx | puppies & kittens: blood transfusions, fluids, remove from GIT; weanling foals: reduce zing in diet, inc dietary copper |