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Toxicology > Blakley #2 > Flashcards

Blakley #2 Flashcards

1
Q

what is metaldehyde

A

a molluscide used to control snails and slugs

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2
Q

absorption of metaldehyde

A

well absorbed in intestine; can become addicting to dogs

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3
Q

metabolism of metaldehyde

A

rapidly metabolized to acetaldehyde

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4
Q

distribution and excretion of metaldehyde

A

readily crosses BBB, metaldehyde is responsible for toxicity, acetaldehyde causes vomiting/tremors and is excreted in urine

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5
Q

mechanism of action of metaldehyde

A

reduces GABA and serotonin levels in brain causing CNS excitation (occasionally depression); depression of medullary respiratory center leads to death

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6
Q

minor mechanisms of metaldehyde

A

gastroenteritis (chemical irritation), brain damage, mild liver damage

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7
Q

clinical manifestations of excitatory syndrome of metaldehyde toxicity

A

salivation, tremors, ataxia, continuous convulsions, opisthotonus, nystagmus (cats), elevated BT

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8
Q

clinical manifestations of depressive syndrome of metaldehyde toxicity

A

emesis, depression, incoordincation, increased RR and HR, cyanosis and coma

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9
Q

PM findings of metaldehyde toxicity

A

non-specific lesions; congestion and mild hemorrhage of liver, kidney and GIT; stomach smells like apple cider, large amount of content

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10
Q

what does the stomach contents of metaldehyde toxicity smell like

A

apple cider from acetaldehyde

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11
Q

diagnosis of metaldehyde toxicity

A

sudden onset of neuro signs, large quantities of pleasant smelling stomach contents, analysis of stomach contents

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12
Q

treatment of metaldehyde toxicity

A

sedation, anesthesia, emetics, fluids (shock/acidosis) +/- activated charcoal (crisis usually over in 24 hours due to rapid elimination)

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13
Q

species susceptibility with strychnine toxicity

A

all mammals are highly susceptible (dogs are the most); secondary poisoning/relay toxicity is common

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14
Q

absorption of strychnine

A

rapidly absorbed; clinical manifestations within 15 minutes to 1 hour

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15
Q

distribution of strychnine

A

can be detected in liver, kidney, brain, blood or stomach contents (stomach contents are best)

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16
Q

metabolism and excretion of strychnine

A

metabolized rapidly by liver with half life of 10 days; excreted in urine and saliva

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17
Q

mechanism of action of strychnine

A

strychnine competitively antagonizes glycine resulting in loss of inhibitory processes and neurological excitation (glycine in the predominant inhibitory neurotransmitter at level of spinal cord and medulla); interferes with post-synaptic inhibitory control at level of spinal cord; also alters K ion gates postsynaptically leading to motor neuron excitability

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18
Q

why does strychnine not interfere with post-synaptic inhibitory control in the brain

A

because it is regulated by GABA, not glycine

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19
Q

clinical manifestations of strychnine toxicity

A

sudden onset, apprehension, nervousness, tenesmus, rigid muscle (especially face), tetanic seizures begin in 15 minutes-2hours (extensor rigidity of all 4 limbs), as more strychnine is absorbed relaxation periods between seizures becomes shorter, seizures can be triggered by external stimuli, apnea (anoxia, coma and death within 1-2 hours)

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20
Q

PM findings of strychnine toxicity

A

no specific lesions because it is a neuro/biochem disturbance; agonal congestion and hemorrhage due to nature of death

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21
Q

diagnosis of strychnine toxicity

A

sudden death in normal healthy dog; analysis of stomach contents, vomitus or liver

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22
Q

treatment of strychnine toxicity

A

emergency treatment, apomorphine (emetic; prior to seizures), gastric lavage with activated charcoal or tannic acid (bind/precipitate strychnine), potassium permanganate, sedation, muscle relaxants

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23
Q

most important treatment for strychnine toxicity

A

sedation

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24
Q

which are the coumarin derivative anticoagulant rodenticides

A

warfarin, brodifacoum, difencoum

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25
Q

which are the indane dione derivative anticoagulant rodenticides

A

diphacinone, chlorophacinone, pindone, valone, bromadiolone

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26
Q

toxicity of anticoagulant rodenticides

A

first generations require repeated exposure for 1-2 weeks; second generation can have problems with a single dose

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27
Q

absorption of anticoagulant rodenticides

A

well absorbed

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28
Q

distribution of anticoagulant rodenticides

A

highly protein bound

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29
Q

metabolism and excretion of anticoagulant rodenticides

A

excreted in urine; warfarin has a half-life of 44 hours; second generations are fat soluble and have longer half lives

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30
Q

mechanism of action of anticoagulant rodenticides

A

complete inhibition of vitamin K epoxide reductase (reduced vitamin K is required for activation of factors 2, 7, 9 and 10)

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31
Q

when does bleeding occur with anticoagulant rodenticide toxicity

A

clotting times will be prolonged 3 days after exposure; bleeding by days 4-5 or later

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32
Q

factors altering toxicity of anticoagulant rodenticides

A

high fat diet, prolonged oral antibiotics (sulfonamides), protein binding drugs, liver disease, prolonged GIT disturbance

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33
Q

clinical manifestations of anticoagulant rodenticide toxicity

A

severe hemorrhage, sudden onset, dyspnea, anemia, melena, rapid irregular HR, hematoms, abortion, proprioceptive deficits and tender abdomen with 2nd generation products

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34
Q

diagnosis of anticoagulant rodenticide toxicity

A

elevated coagulation time, elevated PT/PTT, normal platelet count and WBC count, reduced PCV, thoracocentesis, chemical analysis of blood, liver and urine

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35
Q

PM findings of anticoagulant rodenticide toxicity

A

generalized hemorrhage, mild hepatic necrosis associated with hypoxia from lack of perfusion

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36
Q

treatment of anticoagulant rodenticide toxicity

A

avoid trauma, blood transfusion,vitamin K1 (oral, takes 12 hours), cholestryamine (bile sequestrant to reduce enterohepatic circulation)

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37
Q

how long does vitamin K1 need to be given to 2nd generation anticoagulant rodenticide toxicity animals

A

4-6 weeks; if you shorted treatment they will relapse by 8-9 days later so want to check at 4 (warfarin needs only 1 weeks)

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38
Q

why don’t you treat anticoagulant toxicity with vitamin K3

A

because it requires metabolic activation – epoxide reductase is inhibited by the anticoagulant

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39
Q

what are the toxicokinetics of alpha-naphthyl thiourea (ANTU)

A

rapid absorption, metabolism, and excretion; symptoms within an hour

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40
Q

mechanism of action of ANTU

A

increases permeability of pulmonary capillaries (transudates in airway); cause of death is anoxia from decreased lung perfusion

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41
Q

clinical manifestations of ANTU

A

vomiting, salivation, dyspnea, frothing/coughing, cyanosis, increased HR that sounds muffled, dog sitting position to increase lung volume, schock

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42
Q

PM findings of ANTU

A

massive pulmonary edema; hydrothorax and froth, agonal hemorrhage and congestion

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43
Q

diagnosis of ANTU toxicity

A

history, clinical and pathological changes; chemical analysis needs to be done within 24 hours of death

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44
Q

treatment of ANTU toxicity

A

diuretics, steroids and atropine (all too slow to be clinically significant)

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45
Q

what is fluoroacetate

A

one of the most potent toxic rodenticides, water soluble, colorless, odorless powder

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46
Q

toxicokinetics of fluoroacetate

A

rapidly absorbed, metabolic activation is required so there is about a 1 hour delay before clinical signs

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47
Q

mechanism of action of fluroacetate

A

replaces the acetyl coenzyme A in the Kreb’s cycle; (converted to fluorocitrate, the aconitase enzyme that would normally convert citric acid to isocitric acid is inhibited by fluorocitrate) – cellular respiration and energy production stop due to blocked kreb’s cycle

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48
Q

clinical manifestations of fluoroacetate poisoning (early stages)

A

restlessness, hyperirritability, frenzy, barking

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49
Q

clinical manifestations of fluoroacetate poisoning (late stages)

A

vomiting, diarrhea, tenesmus, urination, defecation, dyspnea, intermittent tonic-clonic convulsions, periods of running (dogs), cardiac arrythmia and fibrillation, vocalization (cat), elevated BT

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50
Q

PM of fluoroacetate poisoning

A

no pathognomonic lesion; agonal hemorrhage and congestion

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51
Q

diagnosis of fluoroacetate poisoning

A

death within 2-12 hours (respiratory failure, cardiac arrythmia and fibrillation), history, clinical and PM

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52
Q

why is analysis of fluoroacetate difficult

A

because it is no longer present as fluoroacetate

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53
Q

treatment of fluoroacetate

A

calcium ketoglutarate can be beneficial to correct the Ca imbalance and ketoglutarate provides and essential energy substrate after the metabolic block

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54
Q

absorption of zinc phosphide

A

reacts with stomach acids to form phosphine gas – instantaneous, gas is readily absorbed

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55
Q

excretion and metabolism of zinc phosphide

A

both parent compound and phosphine gas are eliminated readily

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56
Q

mechanism of action of zinc phosphide

A

irritant and inhibits cytochrome C oxidase

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57
Q

clinical manifestations of zinc phosphide

A

irritation can cause vomiting; 4-5 hours later – depression, tremors, hyperesthesia, seizures, running has been observed, salivation and dyspnea. (colic and bloat in livestock)

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58
Q

PM of zinc phosphide toxicity

A

congested lungs with interlobular edema, gastritis, irritation, tubular degeneration and necrosis of kidney, fatty degeneration of liver, stomach contents may have acetylene or garlic odor

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59
Q

what do the stomach contents smell like with zinc phosphide

A

garlic odor or acetylene

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60
Q

diagnosis of zinc phosphide toxicity

A

analyze stomach contents for zinc

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61
Q

treatment of zinc phosphide toxicity

A

fluids and bicarb to control shock and acidosis; atropine to reduce pulmonary secretions; poor prognosis

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62
Q

what is cholecalciferol

A

a vitamin D product that tends to have toxic irreversible damage (syndrome can be produced by ingestion of rodent baits, vitamin D supplements or excessive levels of vitamin D in feed)

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63
Q

toxicokinetics of cholecalciferol

A

rapid absorption, symptoms within 24 hours, metabolized in liver and excreted in kidney

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64
Q

mechanism of action of cholecalciferol

A

increased absorption of Ca from GIT and enhanced Ca mobilization from bone – hypercalcemia causes conduction problems and metastatic calcification of soft tissues

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65
Q

clinical manifestations of cholecalciferol

A

vomiting, anorexia, diarrhea, tremors, hypoesthesia, depression and lethargy

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66
Q

PM of cholecalciferol

A

with sufficient dose death occurs in 24 hours; calcification in kidney, hemorrhagic gastroenteritis, mineralization, degeneration and necrosis in other organ systems

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67
Q

normal ionophore mechanism of action

A

increases intracellular Na and decreasing intracellular K – alters electrolyte balance of host, bacteria and protozoa (increases propionic/acetic acid ratio thus improving energy utilization)

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68
Q

ionophore mechanism of toxicity

A

K transport is altered in the mitochondria leading to reduced ATP hydrolysis and energy production; possibly also cause increase in Ca intracellularly (heart is very susceptible); as intracellular K decreases, cytotoxicity increases

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69
Q

toxicokinetics of ionophores

A

limited absorption, rapid metabolism, short withdrawal times

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70
Q

species susceptibility differences in ionophore susceptibility

A

horses are the most susceptible, chickens are the least

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71
Q

predisposing factors to ionophore toxicity

A

vitamin E/Se deficiency, T-2 toxin exposure, drug interactions

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72
Q

clinical manifestations of ionophore toxicity (horses)

A

leg weakness progressing to paralysis, sore muscles, staggering, ataxia, reluctant to move, huge increased HR, congested MM, hemoconcentration, hypovolemia, shock, arrythmia, dyspnea, anorexia, sweating, ventral pitting edema (later)

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73
Q

PM of acute sudden death ionophore toxicity

A

no lesions

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74
Q

PM of delayed death ionophore toxicity

A

myopathy and CHF are evident with hydrothorax, ascites, pulmonary edema

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75
Q

diagnosis of ionophore toxicity

A

need to run tests on day 1; myoglobinuria, creatinine phosphokinase, LDH2 (reflects RBC membrane damage), ECG (T wave depression and S-T segment depression), hemoconcentration, tryponin (cardiac specific)

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76
Q

what may chronic monensin toxicity show

A

edema on the feet

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77
Q

treatment of ionophore toxicity

A

muscle damage is permanent; fluids and steroids for shock but be cautious (if kidney damage), mineral oil, diuretics (caution), vitamin E/Se

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78
Q

what species is most affected by salt poisoning

A

swine

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79
Q

what is required for salt poisoning

A

water deprivation and an imbalance of Na and water

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80
Q

when do animals have increased water requirements

A

lactation, renal disease, high salt intake, high protein intake, high environmental temperature, exercise

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81
Q

causes of water deprivation

A

medicated water, frozen water supplies, faulty water system, overcrowding, new surroundings, neglect, electrified water system

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82
Q

mechanism of action of salt poisoning

A

restricted water intake causes the blood and brain Na levels to rise; inhibition of anaerobic glycolysis and energy processes necessary for brain; the levels of ATP necessary to remove Na from brain don’t work; if water is restored Na concentration in blood rapidly declines; thus to maintain osmotic balance water moves into the brain (AA in brain also contribute to its high osmolarity)

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83
Q

clinical manifestations of salt poisoning

A

intermittent tonic-clonic seizures, depression, anorexia, blind, deaf, aimless wandering, circling, opisthotonus, head pressing

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84
Q

clinical manifestations of salt poisoning in cattle

A

diarrhea and anorexia; neuro signs not common

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85
Q

PM of salt poisoning

A

few gross lesions; mild gastric inflammation and ulcers

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86
Q

Histology of salt poisoning

A

eosinophilic meningoencephalitis, cerebral edema and necrosis, macrophage infiltration of cortex, endothelial proliferation of white matter

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87
Q

diagnosis of salt poisoning

A

elevated sodium levels in serum, CSF, brain

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88
Q

treatment of salt poisoning

A

controlled water intake after deprived period could help; no successful treatment – just take to butcher

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89
Q

what do many fertilizers contain

A

urea (46-0-0) and ammonium (34-0-0)

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90
Q

how do you differentiate whether fertilizer contained urea or nitrate based on the animal

A

urea will be hydrolyzed in the gut causing increased rumen pH and normal colored blood; nitrate fertilizer causes chocolate brown blood and normal pH

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91
Q

species susceptibility of urea poisoning

A

only ruminants are susceptible; horses to a certain extent; (all species susceptible to ammonium ion)

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92
Q

how is urea utilized in the rumen

A

it is hydrolyzed by rumen microflora to form ammonia and carbon dioxide by the urease enzyme (not regulated); ammonia is incorporated by rumen microflora into protein; excess ammonia is transported to liver where it is converted back to urea and excreted in urine (can also be recycled into AA)

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93
Q

when does urea toxicity result

A

when the capacity of the recycling system for ammonia is exceeded – high levels of ammonia result in toxicity

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94
Q

what are the optimal conditions for urea hydrolysis

A

pH of 7.7-8.0 and temperature of 49C

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95
Q

predisposing factors to urea toxicity

A

no previous urea exposure (naive microflora), fasting, starvation, dehydration (can’t excrete in urine), hepatic insufficiency, high roughage diet (more optimal pH), elevated BT, stress, disease ((Young are less susceptible))

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96
Q

biochemical changes in urea toxicity

A

excess ammonia enters blood causing and increased pH and inhibition of the Kreb’s cycle –> compensatory glycolysis to elevated blood glucose and lactic acid –> drop in pH; inhibition of energy processes cause increase K release from cells with cell membrane damage and thus cardiotoxicity; ammonia also has strong irritant effect on lungs

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97
Q

clinical manifestations of urea toxicity

A

onset can be within 10 minutes; restlessness, belligerant periods, head pressing, hyperesthesia, tremors, twitching, spasms, eyelids, tonic seizures, opisthotonus, saw-horse stance, rumen stasis, bloat, groaning, grinding teeth, no diarrhea, frothy salivation (lose urea through saliva), incoordination, recumbency of front end, dyspnea from pulmonary edema, jugular pulse, hyperthermia

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98
Q

what are the most notable signs of urea toxicity

A

GIT signs; rumen stasis, bloat, groaning, grinding teeth, no diarrhea, frothy salivation (lose urea through saliva)

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99
Q

PM of urea toxicity

A

rumen pH greater than 7.5 (do ASAP because ammonia evaporates), pulmonary edema, ammonia odor, catarrhal gastroenteritis, petechial hemorrhage

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100
Q

diagnosis of urea toxicity

A

measurement of blood and rumen pH; also ammonia levels

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101
Q

treatment of urea toxicity

A

administer vinegar and cold water (make rumen environment less ideal for urease enzyme)

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102
Q

factors related to plant growth that increase the likelihood of plant poisoning

A

age of plant, growth conditions, portion of plan, plant injury, post harvest storage, plant species, soil condition, fall sprouting

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103
Q

what toxic compounds are present in oak

A

gallotannins and polyhydroxyphenolic compounds

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104
Q

where are toxic compounds present in oak

A

leaves and acorns

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105
Q

mechanism of action of oak toxicity

A

tannins act as astringents to destroy epithelial cells of GIT and renal

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106
Q

clinical manifestations of oak toxicity

A

GIT signs first then renal insufficiency; anorexia, dullness, colic, rumen stasis, dehydration, emaciation, constipation then hemorrhagic diarrhea, hematuria, polyuria, ascites and hydrothorax, icterus

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107
Q

PM of oak toxicity

A

GIT ulcers, enteritis, edema, ascites, tubular nephrosis and necrosis, acorns in rumen, hyaline membrane

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108
Q

clinical pathology of oak toxicity

A

elevated BUN and creatinine, elevated liver enzymes, altered electrolytes, USG low, hematuria, proteinuria

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109
Q

treatment of oak toxicity

A

add CaOH to grain ration to precipitate gallotannins in gut and prevent absorption; reduce access, supplemental feed

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110
Q

diagnosis of oak toxicity

A

GI problems, kidney problems, time of year, history

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111
Q

mechanism of action of red maple toxicity (acer rubrum)

A

component of leaves causes oxidative damage characterized by intravascular hemolysis and methemoglobinemia

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112
Q

clinical manifestations of red maple toxicity

A

weakness, increased RR and HR, pale, hemoglobinuria, hemoglobinemia, jaundice, anemia, methemoglobinemia, heinz bodies

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113
Q

treatment of red maple toxicity

A

non are very effective, especially if methemoglobinemia is present; blood transfusion, fluids, peritoneal dialysis

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114
Q

susceptibility of species to nitrate/nitrite poisoning

A

primarily a problem in ruminants; monogastrics have a limited ability to convert nitrate to nitrite (unlikely to develop toxicity) but can see with consumption of brines containing nitrite

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115
Q

sources of nitrate

A

forage crops, nitrate fertilizer, contaminated water, numerous weeds – both feed and water sources will produce additive effects (10x more available in water)

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116
Q

factors influencing nitrate accumulation in plants

A

high soil nitrate, plant species, part of plant (stalk and leaves are higher), age of plant (immature>mature), drought, light and length of day (nitrate reductase requires light), temperature (frost reduces nitrate metabolism), soil pH, plant disease, herbicide application, aeration of soil, Mo, S and P deficiency (needed for reductase), late season sprouting

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117
Q

mechanisms of action of nitrate/nitrite toxicity

A

both are toxic but nitrite ion is more toxic; nitrate converted to nitrite in rumen; under normal circumstances nitrite is converted to ammonia or AA

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118
Q

what is the rate limiting step of nitrate/nitrite metabolism

A

metabolism of nitrite to ammonia/AA

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119
Q

nitrate effects

A

Cl displacement causing hypochloremia and alkalosis, diuresis (dehydration), GIT irritation, iodine displacement (goitre)

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120
Q

nitrite effects

A

methemoglobin formation (hemoglobin oxidation), vasodilation, NO2 gas formation causing pneumonitis, vitamin A inactivation

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121
Q

how does death occur with nitrate/nitrite toxicity

A

tissue anoxia

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122
Q

clinical manifestations of nitrate/nitrite toxicity

A

nitrate causes gastroenteritis, abdominal pain, diarrhea and salivation; nitrite causes severe manifestations in 4 hours with death in 12-24 as a respiratory distress syndrome (cyanosis, rapid weak HR, dyspnea, muddy chocolate brown MM, urination, incoordination, muscle weakness, abortion, bloat, coma, convulsion, death

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123
Q

PM of nitrate/nitrite toxicity

A

mild gastroenteritis, chocolate brown discoloration of most tissues, petechial hemorrhage in heart and trachea, poorly clotting blood, and mild pulmonary edema

124
Q

susceptibility of adult versus fetus to nitrate/nitrite toxicity

A

fetal hemoglobin is more readily converted to methemoglobin therefore fetus is more susceptible than adult

125
Q

diagnosis of nitrate/nitrite toxicity

A

feed analysis, water analysis, methemoglobin levels are best measurement

126
Q

treatment of nitrate/nitrite toxicity

A

methylene blue is best (if you overdose though you end up with more methemoglobin), vasoconstrictors, vitamin A supplementation, mineral oil

127
Q

prevention of nitrate/nitrite toxicity

A

dilute high nitrate feeds, feed highly fermentable carbohydrate ration

128
Q

what are hydrocyanic acid or prussic acid poisoning associated with the ingestion of (cyanide poisoning)

A

ingestion of plants containing cyanogenic glycosides

129
Q

what is the toxic principle of plants containing cyanogenic glycosides

A

HCN – small molecule that is well absorbed from resp and GI

130
Q

sources of cyanide

A

plants or pits of various fruits; peaches, cherries, almonds, sorghum, sudan grass, cherry leaves, arrow grass, white clover

131
Q

factors affecting cyanide accumulation

A

what changes nitrate a little bit, changes CN a lot; wilting, trampling, frost, drought, herbicide, fertilizer, age of plants (younger contain more), declining day length

132
Q

species susceptibility of cyanide poisoning

A

ruminants > monogastrics because greater capacity to metabolize cyanogenic glycosides (horses and swine are less susceptible)

133
Q

metabolism of CN

A

80% is metabolized in liver by rhodanase enzyme, CN accepts sulfur molecule to form thiocyanate (SCN); 15% of CN can be excreted unmetabolized in lungs or urine

134
Q

when does CN toxicity occur

A

when the natural detoxification system (SCN) is exceeded or the source of sulfur is depleted

135
Q

what smell can be detected in exhaled gases or rumen contents of CN poisoned animals

A

bitter almond smell

136
Q

mechanism of action of CN toxicity

A

high binding affinity for ferric compounds; forms a stable inactive complex with cytochrome oxidase thus stopping cellular respiration leading to acute histotoxic anoxia

137
Q

clinical manifestations of cyanide toxicity

A

life threatening manifestations within 15 minutes to an hour, excitement, rapid breathing to dyspnea, muscle twitching, tremors, staggering, terminal anoxic convulsions, opisthotonus, nystagmus, pupil dilation, cyanosis, bloat, blood is bright cherry red

138
Q

what color is the blood in cyanide toxicity

A

bright cherry red (highly oxygenated but no oxygen change occurs)

139
Q

PM of cyanide toxicity

A

MM are congested and bright red, gastroenteritis, unclotted blood often, endocardial hemorrhage and congestion, bitter almond smell in rumen (with chronic poisoning can observe axonal degeneration and demyelination)

140
Q

diagnosis of cyanide poisoning

A

acute toxicity with sudden onset of neuro symptoms and confirmed by measurement of cyanhemoglobin in heparinized blood (analysis needs to be within 4 hours because CN will dissipate); can also look at rumen contents, plant, liver and muscle; field test for CN with color reaction

141
Q

treatment of cyanide poisoning

A

sodium thiosulfate IV (thiosulfate reacts with cyanhemoglobin to produce thiocyanate and functional hemoglobin; stress of handling often kills more than helps

142
Q

goitrogenic syndrome of chronic cyanide poisoning

A

cyanide is thyrotoxic so observe goitre in lambs

143
Q

sorghum cystitis of chronic cyanide poisoning

A

horses consuming sorghum or sudan grass develop a syndrome characterized by neuronal degeneration (neuro and nephro); ataxia (axonal degeneration and demyelination), cystitis, urinary incontinence, pyelonephrities, joint fixation in fetus

144
Q

livestock oxalate poisoning is caused by

A

ingestion of plants containing oxalates and produces syndrome with hypocalcemia and renal failure

145
Q

pet oxalate poisoning is caused by

A

ingestion of ethylene glycol producing syndrome with metabolic acidosis and renal failure

146
Q

plants that contain Na or K salts of oxalates

A

rhubarb leaves, beet leaves, halogeton, greasewood

147
Q

susceptibility to plant oxalate poisoning

A

sheep are more susceptible than cattle; pregnant/lactating or hungry animals that eat large quantities are more susceptible

148
Q

toxicokinetics of plant oxalate poisoning

A

Na and K oxalate salts are well absorbed; Ca salts are poorly absorbed (can feed CaOH to bind to Na/K oxalates in gut); Na/K salts complex with Ca in blood, rumen wall or capillaries

149
Q

how does rumen normally handle Na/K oxalate salts

A

microflora metabolize the two carbon oxalate molecules to form CO2 and bicarb – when this is overwhelmed oxalate salts are absorbed

150
Q

factors influencing plant oxalate toxicity

A

dose, rate of ingestion, type of tumen microflora (can adapt), high Ca is protective in feed (so is low pH), cobalt deficiency increases toxicity, water consumption causes increased absorption

151
Q

mechanism of action of plant oxalate toxicity

A

hypocalcemia from formation of Ca oxalate; oxalate crystals damage renal epithelium, capillaries and rumen wall

152
Q

clinical manifestations of plant oxalate toxicity

A

milk fever 2-6 hours after ingestion (paresis, muscle weakness, twitching, increased HR), osteodystrophia fibrosa (chronic ingestion by horses), nephrosis, urinary calculi, vascular damage, rumen dysfunction

153
Q

diagnosis of plant oxalate toxicity

A

low calcium, reduced PCV, elevated BUN

154
Q

PM of plant oxalate toxicity

A

ascities, hydrothorax, oxalate crystal striations in kidney, urinary calculi, rumenitis

155
Q

treatment of plant oxalate toxicity

A

oral administration of CaOH to precipitate in GIT and calcium borogluconate with caution

156
Q

prevention of plant oxalate toxicity

A

dietary supplementation with Ca, don’t feed to pregnant/lactating

157
Q

ethylene glycol mechanism of action

A

first 2-4 hours has a narcotic effect, next 24 hours ethylene glycol is metabolized to aldehydes and acids (ultimately oxalic acid)

158
Q

clinical manifestations of ethylene glycol toxicity

A

alcohol intoxication in first 4 hours (depression, vomiting, ataxia, incoordination, diuresis); metabolic acidosis leads to increased HR and RR; by 48 hours, uremic state due to renal damage, elevated BUN and AG, reduced blood pH, proteinuria, hematuria, hyperglycemia

159
Q

when is it crucial to diagnose ethylene glycol toxicity

A

prior to irreversible kidney damage; do a blood gas

160
Q

PM of ethylene glycol toxicity

A

gastritis, pale swollen kidney with oxalate striatins, mild pulmonary edema

161
Q

diagnosis of ethylene glycol

A

blood gas, kits to detect ethylene glycol in blood

162
Q

treatment of ethylene glycol

A

4-methylprazol in dogs only (inhibits alcohol dehydrogenase and prevents oxalate formation); butylene glycol for cats; fluids and bicarb for acidosis and shock, activated charcoal very early on

163
Q

which fungus produces aflatoxin

A

aspergillus

164
Q

which plant is aflatoxin (mycotoxin) associated with

A

peanuts

165
Q

mechanism of action of aflatoxin

A

inhibits protein synthesis by affecting both mRNA synthesis and DNA synthesis

166
Q

target organ of aflatoxin

A

liver

167
Q

clinical manifestations of acute aflatoxin toxicity

A

depression, poor production, anorexia, rumen stasis, ataxia, icterus and hematomas

168
Q

clinical manifestations of chronic aflatoxin toxicity

A

reduce feed efficiency, weight gain and milk production, anorexia, icterus, anemia, ascites, large abdomen

169
Q

PM of acute aflatoxin toxicity

A

centrilobular hepatic necrosis, bile duct proliferation and fibrosis, hemorrhage, ascites

170
Q

clinical pathology of aflatoxin toxicity

A

mild anemia, elevated liver enzymes, increased bilirubin, increased PT, decreased BUN, reduced CMI (decreased WBC)

171
Q

diagnosis of aflatoxin toxicity

A

chemical analysis of feed, possibly tissues (bile, liver kidney)

172
Q

residue concerns with aflatoxin toxicity

A

rapidly cleared in 3-4 days; secreted in milk at relevant levels; carcinogen

173
Q

treatment of aflatoxin toxicity

A

remove from feed; possibly vitamin E/Se

174
Q

what fungus produces zearalenone mycotoxin

A

fusarium

175
Q

what crop is zearalenone associated with

A

corn – also present in many types of grain

176
Q

zearalenone toxicokinetics

A

well absorbed, rapid metabolism, enterohepatic recycling prolongs retention, secreted in milk

177
Q

mechanism of action of zearalenone toxicity

A

binds receptors for estradiol causing estrogenic effects; inhibits secretion and release of FSH leading to inhibition of follicle maturation

178
Q

clinical manifestations of zearalenone toxicity

A

older cattle and swine are more resistant; infertility, anestrus, stillbirth, vulvovaginitis(swine), vaginal/rectal prolapse (cattle),pseudopregnancy, early embryonic death, repeat breeding

179
Q

diagnosis of zearalenone

A

based on clinical signs of estrogenic effects; typically a herd problem

180
Q

treatment of zearalenone

A

remove from contaminated feed; repair prolapses, prostaglandin F2 alpha will reduce the CL

181
Q

residue concerns with zearalenone toxicity

A

not a concern

182
Q

fungus that produces trichothecene mycotoxin

A

fusarium

183
Q

3 most common metabolites of trichothecene mycotoxins in canada

A

T-2 toxin (5x more toxic than DON), DAS, and vomitoxin/DON (least toxic)

184
Q

species susceptibility to trichothecene mycotoxins

A

pigs and horses are more susceptible than cattle

185
Q

mechanism of action of trichothecene mycotoxins

A

potent inhibitors of protein synthesis, inhibit DNA/RNA synthesis, directly cytotoxic (destroy lymphocytes), immunosuppressive, irritation, vomitoxin crosses BBB and activates emetic centers

186
Q

clinical manifestations of trichothecene mycotoxin toxicity

A

feed refusal is presenting complaint; dermal necrosis, gastroenteritis, hemorrhage, leukopenia, embryotoxic, abortion, weakness, ataxia, depression

187
Q

metabolism and excretion of trichothecene mycotoxins

A

rapid metabolism and excretion with residues not being a major concern

188
Q

diagnosis of trichothecene mycotoxins

A

analysis of feed

189
Q

treatment of trichothecene mycotoxin toxicity

A

remove from feed and symptomatic; antibiotics for secondary infections, treat ulcers, fluids

190
Q

fungus that ergot is produced by

A

claviceps;

191
Q

what plants are trichothecene mycotoxins in

A

brome grass, sedge grass, rye, wheat, barley, oats, triticale

192
Q

what is the most sensitive indicator of ergot exposure

A

agalactia associated with reduced prolactin production and mammary gland development (persists for entire lactation)

193
Q

what syndrome is associated with higher levels of ergot contamination

A

convulsive

194
Q

mechanism of action of ergot toxicity

A

induces contraction of smooth muscles;vasoconstriction of arteries; alpha-adrengergic blocking effect

195
Q

toxicokinetics of ergot

A

absorption orally is slow and incomplete, rapid metabolism, excreted in bile (reaches steady state with chronic exposure)

196
Q

convulsive syndrome of ergot toxicity manifestation

A

CNS stimulation, hyperexcitability, tremors, hypermetria, ataxia, belligerance, convulsions

197
Q

gangrenous syndrome of ergot toxicity manifestations

A

follows prolonged exposure at lower levels; unthrifty appearance due to vasoconstriction of rumen wall causing decreased VFA absorption, lameness in hindlimbs, elevated HR and RR, reduced milk production

198
Q

effect of ergot toxicity late in gestation

A

inhibitory effects on prolactin leading to agalactia and neonatal starvation; horses are most susceptible

199
Q

diagnosis of ergot

A

clinical signs and feed analysis

200
Q

treatment of ergot toxicity

A

remove from contaminated feed

201
Q

fungus associated with ochratoxin

A

aspergillus, penicllium

202
Q

primary target organ of ochratoxin

A

kidney

203
Q

mechanism of action of ochratoxin

A

binds to proteins and reduces synthesis; alters carbohydrate metabolism; inhibits carboxypeptidase; reduces t+mRNA synthesis; increases free radical production

204
Q

clinical manifestations of ochratoxin

A

uremic syndrom, anorexia, vomiting, diarrhea, dehydration, depression, PU/PD, immunosuppression, teratogenicity

205
Q

clinical pathology of ochratoxin

A

elevate PCV, BUN and serum creatinine, proteinuria, glucosuria, casts, elevated liver enzymes

206
Q

PM of ochratoxin

A

nephrosis, pale swollen kidneys, interstitial fibrosis/necrosis, tubular swelling and atrophy, thickened basement membranes, necrosis of liver, gastritis with possible ulcers

207
Q

fungus that produces dicoumarol

A

penicillium

208
Q

what plant is dicoumarol associated with

A

moldy sweet clover

209
Q

mechanism of action of dicoumarol

A

competes for the same receptor as vitamin K thus inhibiting synthesis of vitamin K dependent coagulation factors (prothrombin, 7, 9, 10)

210
Q

susceptibility to dicoumarol

A

influenced by protein binding; cattle are most susceptible

211
Q

toxicokinetics of dicoumarol

A

well absorbed, readily crosses placent, half-life of 54 hours in cattle, 23 hours in sheep; blood levels decline rapidly while liver levels remain elevated for longer

212
Q

clinical manifestations of dicoumarol

A

massive hemorrhage, animals continue to eat until late stage, HR and RR elevated, pale MM, prolonged CRT, hematomas, abortion (fetus is more susceptible), neonatal death, CNS disturbance, dyspnea

213
Q

clinical pathology of dicoumarol

A

anemia, normal WBC, elevated clotting time, elevated prothrombin time

214
Q

diagnosis of dicoumarol

A

elevated prothrombin time, analyze tissues for dicoumarol (dicoumarol can pass in milk)

215
Q

treatment of dicoumarol

A

remove suspected feed (dilution is ineffective), blood transfusion, vitamin K

216
Q

recommendations for feeding sweet clover to cattle

A

don’t feed to pregnant animals in last trimester, feed rotation, routine blood monitoring, withdrawal of 6 weeks before dehorning etc., don’t ship cattle until clotting times have returned to normal

217
Q

what fungus is fumonisin (mycotoxin) produced by

A

fusarium (corn)

218
Q

susceptibility to fumonisin toxicity

A

horses are most susceptible

219
Q

mechanism of action of fumonisin toxicity

A

interfere with biosynthesis of sphingolipids causing decreased membrane stability

220
Q

clinical manifestations of fumonisin toxicity in horses

A

equine leukoencephalomalacia – depression, blindness, ataxia, circling, wandering, facial paralysis, swallowing problems, head pressing, death in 1-3 days

221
Q

clinical manifestations of fumonisin toxicity in pigs

A

dyspnea, cyanosis, weakness, death in a week

222
Q

diagnosis of fumonisin toxicity

A

elevated liver enzymes, bilirubin, cholesterol and BUN; WBC and protein in CSF

223
Q

PM of fumonisin toxicity

A

necrosis and malacia of cerebral white matter, hemorrhage in white matter, liver necrosis and apoptosis, kidney nephrosis, pulmonary edema (pigs)

224
Q

treatment of fumonisin toxicity

A

none specifically; neuro damage is irreversible

225
Q

toxicokinetics of oil poisoning

A

most are lipophilic and are readily absorbed by all routes including respiratory

226
Q

mechanism of action of oil poisoning

A

irritation, GIT dysfunction through stimulation or microorganism alteration, bonemarrow suppression

227
Q

clinical manifestations of oil poisoning

A

aspiration pneumonia (oil is 100 fold more toxic if inhaled so causes ciliary and cough function to not work), lipid pneumonia (WBC skyrocket), bloat, anorexia, weight loss, ketosis, oil smell in rumen (float contents), dyspnea, ataxia, incoordination, abortion, elevated BT

228
Q

clinical pathology of oil poisoning

A

leukopenia followed by a neutrophilia (use to tell when exposed), anemia, marrow depression, elevated BUN/liver enzymes

229
Q

PM of oil poisoning

A

evidence of oil in rumen, bloat, GIT irritation, mild degeneration of liver, nephrosis, pulmonary congestion and consolidation, pulmonary abscesses, fibrinous pleuritis, dermal irritation

230
Q

other concerns regarding oil poisoning

A

milk taint and meat residues, low vitamin E/A, impaired reproduction, cancer, endocrine disruption

231
Q

treatment of oil poisoning

A

activated charcoal, mineral oil, antibiotics for secondary infection; bathe wild life with detergent to remove oil and prevent hypothermia; do not induce vomiting

232
Q

toxicokinetics of coal tar and phenol compounds

A

well absorbed orally and reasonably through the skin; metabolized in liver by glucoronidation so cats are more susceptible

233
Q

mechanism of action of coal tar and phenol compounds

A

protoplasmic toxicant causes liver necrosis and renal tubular necrosis; ingestion of clay pigeons by swin results in hemorrhagic hepatitis

234
Q

clinical manifestations of coal tar and phenol compounds

A

sudden death with high dose; low to moderate dose – anorexia, depression, weakness, tremors, jaundice, secondary anemia, possible photosensitization

235
Q

PM of coal and phenol compounds

A

necrosis and ulceration of skin, enlarged pale kidney with tubular necrosis, centrilobular degeneration and necrosis of liver, icterus

236
Q

clinical pathology of coal and phenol compounds

A

proteinuria, hematuria, epithelial cells/casts, elevated liver enzymes

237
Q

diagnosis of coal and phenol compounds

A

pathological and circumstantial information

238
Q

treatment of coal and phenol compounds

A

activated charcoal and wash skin with detergent; gastric lavage; vitamin E

239
Q

two groups of chemicals in polyhalogenated biphenyls

A

PBB (more toxic) and PCB

240
Q

why were PBB and PCB banned

A

embryotoxic, teratogenic, carcinogenic, immunosuppressive, residues, potent enzyme inducers

241
Q

mechanism of action of PBB and PCB

A

enzyme induction; degenerative and membrane changes in variety of tissues

242
Q

clinical manifestations of PBB/PCB toxicity in dairy cattle

A

insidious vague onset, weight loss, reduced milk production, abnormal hoof development, atrophy of udder, increased urination and lacrimation, hematomas, thrombocytopenia, abscesses, metritis, abortion, prolonged gestation, alopecia, chloroacne

243
Q

PM of PBB/PCB toxicity

A

emaciation, thymic atrophy, heptaic fatty change, renal tubular degeneration, ascites

244
Q

treatment of PBB/PCB toxicity

A

slaughter and disposal because of residue and reproductive effects; burning is best way

245
Q

factors influencing fluoride toxicity

A

amount ingested, duration of exposure, solubility, age (young and fetus are more susceptible), nutritional status (high Ca protective), stress

246
Q

toxicokinetics of fluoride toxicity

A

well absorbed, cumulative poison (predisposition to calcified tissues), fetus accumulates

247
Q

mechanism of action of fluoride toxicity

A

delays and alters normal mineralization of bones and teeth

248
Q

clinical manifestation of acute fluoride toxicity

A

symptoms within 30 minutes, irritation, colic, saliva, vomiting, hemorrhagic gastroenteritis, stiffness, muscle weakness, convulsions, cardiac failure

249
Q

chronic fluoride toxicity manifestations

A

lameness, stiffness, unthrifty, mottled brownb and uneven tooth enamel, exostoses, lapping of water due to dental pain

250
Q

diagnosis of fluoride toxicity

A

history of lameness and dental problems; usually a herd problem

251
Q

treatment of fluoride toxicity

A

prevent with administration of aluminum salts at 10x the level of fluoride

252
Q

characteristics of ammonia gas

A

strong base and highly irritant/caustic; generated from sewage pits or fertilizer with no smell

253
Q

mechanism of action of ammonia gas

A

ammonium hydroxide is formed in lungs causing damage

254
Q

manifestations of acute exposure to ammonia gas

A

coughing, dyspnea, pulmonary edema, lacrimation, poultry with opacity in eyes (blinding)

255
Q

treatment of ammonia gas toxicity

A

improve ventilation

256
Q

nitrogen oxide gases characteristics

A

highly toxic, NO2 and N2O4 are at equilibrium with each other

257
Q

mechanism of action of nitrogen oxide gas toxicity

A

react with moist membranes of lung tissue to form nitric acid –> caustic properties of nitric acid cause irritation, pulmonary edema and direct alveolar damage; methemoglobin can also be produced

258
Q

clinical manifestation of nitrogen oxide gas toxicity

A

dyspnea, coughing, salivation, lacrimation, reddened MM, bronchitis, emphysema, secondary bacterial infection

259
Q

treatment of nitrogen oxide gas toxicity

A

improve ventilation

260
Q

where are sulfur oxide gases produced

A

industrial sources such as high sulfur coal or oil combustion

261
Q

mechanism of action of sulfur oxide gas toxicity

A

sulfur reacts with water in lungs to form sulfuric acid that has a caustic effect leading to irritation, pulmonary edema, hemorrhage and emphysema

262
Q

clinical manifestations of sulfur oxide gas toxicity

A

lacrimation, salivation, coughing, bronchoconstriction, cyanosis, red MM

263
Q

PM of sulfur oxide gas toxicity

A

pulmonary edema, emphysema, atelectasis, hemorrhage, fibrosis, secondary bacterial pneumonia

264
Q

treatment of sulfur oxide toxicity

A

remove from contaminated area

265
Q

characteristics of hydrogen sulfide gas

A

extremely toxic; one breath can kill; smells like rotten eggs (but rapidly destroys sense of smell)

266
Q

what four major gases do sewage pits produce

A

hydrogen sulfide, ammonia, carbon dioxide, methane

267
Q

mechanism of action of hydrogen sulfide (3)

A

irritation (reacts with Na to for Na2S that produces pulmonary edema); enzyme inhibition of cytochrome oxidase enzyme causing cellular respiration to stop (hypoxia); binds with hemoglobin to produce sulfhemoglobin

268
Q

clinical manifestations of hydrogen sulfide gas

A

coughing, lacrimation, pulmonary edema,dyspnea, bronchoconstriction, cyanosis, anoxic terminal convulsions

269
Q

PM of hydrogen sulfide gas toxicity

A

few gross lesions; may smell hydrogen sulfide on tissues

270
Q

treatment of hydrogen sulfide gas toxicity

A

ventilation, oxygen

271
Q

mechanism of action of carbon monoxide

A

rapidly absorbed and reacts quickly with hemoglobin to form carboxyhemoglobin

272
Q

clinical manifestations of carbon monoxide toxicity

A

CNS excitation to depression, disorientation, muscle weakness, elevated HR/RR, dyspnea, bright red blood and MM (dissipates over time), coma and death

273
Q

treatment of carbon monoxide toxicity

A

high levels of oxygen to displace CO from hemoglobin; avoid respiratory stimulants because increase oxygen demand

274
Q

examples of anionic detergents

A

laundry detergent, dishwasher detergent, shampoo

275
Q

anionic detergent toxicity and absorption

A

slight-moderate toxicity; well absorbed orally, does not penetrate intact skin;

276
Q

clinical manifestations of anionic detergent toxicity

A

dermal irritation and blistering can occur; vomiting and diarrhea; ocular exposure can cause corneal erosion and opacity

277
Q

treatment of anionic detergent toxicity

A

oral administration of milk/water to dilute, activated charcoal, wash, alkalinization of urine to prevent renal damage

278
Q

examples of cationic detergents

A

fabric softeners and sanitizers; highly toxic

279
Q

absorption of cationic detergents

A

well absorbed orally but poor dermal absorption

280
Q

clinical manifestation of cationic detergent toxicity

A

vomiting, salivation, muscle weakness, fasciculations, CNS or resp depression, corrosive damage to MM, hairloss, skin ulcers

281
Q

treatment of cationic detergent toxicity

A

milk or egg whites, activated charcoal, saline cathartic, fluids; emetics are NOT recommended

282
Q

non-ionic detergents

A

mild irritation and low toxicity; diarrhea and vomiting, treat with milk or water

283
Q

what molecule does bleach contain

A

sodium hypochlorite – not very stable molecule

284
Q

manifestations of bleach

A

corrosive on skin and MM; oxidative damage; reacts with stomach acid to produce chlorine gas that animal can inhale causing pulmonary edema (dyspnea, shallow breathing, cyanosis) – bleach also can react with ammonia to make chloramine gas

285
Q

treatment of bleach exposure

A

wash, milk of magnesia, milk or water; emetics are contraindicated

286
Q

long term effects of bleach exposure

A

pulmonary fibrosis, esophageal stenosis, secondary infections

287
Q

what body systems does ethanol effect

A

GIT and CNS

288
Q

effects of isopropanol

A

severe CNS depression within 1 hour, respiratory depression; acetone the primary metabolite produces a ketosis

289
Q

treatment of isopropanol toxicity

A

emetics are useful within 1-2 hours of ingestion; fluids with bicarb; activated charcoal in INEFFECTIVE

290
Q

mechanism of action of methanol

A

metabolized by alcohol dehydrogenase to formaldehyde then formic acid

291
Q

clinical signs of methanol

A

CNS depression, ataxia, hypothermia, respiratory depression

292
Q

toxicokinetics of pine oils and turpentine

A

readily absorbed, can be detected on breath, metabolized by liver with glucoronidation (cats more susceptible)

293
Q

clinical signs of pine oils exposure

A

erythema on exposed MM, tearing and photosensitivity with eye exposure (+inflammation), weakness, CNS depression, ataxia, nausea, salivation, bloody vomiting, aspiration pneumonia can be subsequent to vomiting, hypotension

294
Q

specific signs observed in cats with pine oil exposure

A

pulmonary edema, centrilobular hepatic necrosis, renal cortical necrosis

295
Q

treatments of pine oil and turpentine exposure

A

milk, egg whites, water; activated charcoal and washing; emetics are contraindicated

296
Q

Naphthalene toxicity (moth balls)

A

cats are most susceptible;

297
Q

Naphthalene clinical signs

A

vomiting, methemoglobinemia, hemolytic heinz body anemia, hemoglobinuria, liver and kidney damage

298
Q

treatment of naphthalene toxicity (moth balls)

A

emesis, activated charcoal, saline cathartic, methylene blue

299
Q

Para-1,4-dichlorobenzene toxicity (moth ball)

A

insecticide; vomiting, pain, tremors, seizures; liver and kidney damage

300
Q

treatment of para-1,4-dichlorobenzene toxicity

A

activated charcoal, symptomatic, sedation

301
Q

what do most drain and oven cleaners contain

A

Na and K hydroxide

302
Q

effect of drain and oven cleaners

A

extremely toxic to skin and MM – coagulation to liquefactive necrosis; can have severe necrosis of esophagus leading to stricture

303
Q

treatment of drain and oven cleaner exposure

A

diluted vinegar to neutralize base; emetics and gastric lavage are contraindicated

304
Q

toxic agent in matches and fireworks

A

potassium chlorate – strong oxidizing agent

305
Q

clinical manifestation of matches and firework exposure

A

vomiting, CNS depression, cyanosis, intravascular hemolysis, methemoglobinuria

306
Q

treatment of matches and firework exposure

A

vitamin C – slow acting; emetics and gastric lavage

307
Q

what other than potassium chlorate do fireworks contain

A

nitrate and perchlorate salts that can cause GIT irritation, vomiting, salivation, pain

Toxicology (4 decks)

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