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Toxicology ME I

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
Created by: shelbell8389



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