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Exam one Flashcards

1
Q

What is the difference between drugs and poisons?

A

the dose

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2
Q

What are xenobiotics?

A

foreign chemicals the body doesn’t produce (ex: drugs and poisons)

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3
Q

What is a poison/toxicant?

A

any substance that when introduced to body can interfere with life processes or biological functions

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4
Q

How is toxicity measured in mammals?

A

LD50 in mg/kg body weight

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5
Q

How is toxicity measured in birds?

A

LC50 in mg/kg feed

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6
Q

How is toxicity measured in fish?

A

LC50 in mg/L h20

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7
Q

What is acute toxicity?

A

effect of a single dose or multiple doses within 24 hours

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8
Q

What is subacute toxicity?

A

effect of daily exposure from 1-30days

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9
Q

What is chronic toxicity?

A

daily exposure for 3 months or more

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10
Q

What is the chronicity factor?

A

ratio between acute LD50 and chronic LD50

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11
Q

What is the highest nontoxic dose?

A

largest dose that does not result in undesirable alterations - similar to maximum tolerated dose or minimal toxic dose

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12
Q

What is the toxic dose low?

A

lowest dose that produces toxic alterations but administering twice does not result in death

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13
Q

What is the toxic dose high?

A

dose that produces toxic alterations and administering twice the dose results in death

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14
Q

What is the no effect level?

A

amount of chemical that can be ingested without causing any deaths or illness for any animals in stated period

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15
Q

What is LD0?

A

highest dose that does not cause death

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16
Q

What is LD50?

A

dose that kills 50% of animals in group

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17
Q

What is LD100?

A

lowest dose that kills all animals in a group

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18
Q

How do you measure therapeutic index?

A

LD50/ED50 smaller value > smaller safety margin

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19
Q

What are the most important routes of toxins?

A

oral, dermal, inhalation

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20
Q

What is lethal synthesis? Examples?

A

when the metabolite is more toxic than parent compound ex: organophosphate, ethylene glycol

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21
Q

What is the most efficient barrier in the body? Least?

A

most = BBB least = placenta

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22
Q

Who assesses drugs?

A

FDA

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23
Q

Who assesses chemicals?

A

EPA

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24
Q

What is the equation for the standard safety margin?

A

(LD1/SD99 - 1) x 100

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25
Q

What is the most important aspect when dealing with toxicosis?

A

accurate or confirmed diagnosis

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26
Q

What are the criteria of diagnosis?

A

case history, clinical signs, postmortem findings, chemical analysis, lab animal tests

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27
Q

What drugs are used to induce emesis when indicated?

A

syrup of ipecac (1/2-2tsp) or hydrogen peroxide 3% (1-2ml/kg)

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28
Q

What are the 4 steps of the treatment of toxicosis?

A
  1. supportive/symptomatic treatment
  2. removal of poison
  3. specific/antidotal treatment
  4. observation
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29
Q

What is the best supportive treatment for respiration?

A

tracheostomy and artificial respiration

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30
Q

What can be given as a bronchodilator?

A

aminophilline

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31
Q

What is the supportive treatment for the cardiovascular system?

A

blood/plasma transfusion, fluids for hypovolemia, cardiac stimulants

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32
Q

What drugs can be given as cardiac stimulants?

A

10% calcium gluconate IV, glucagon IV, digoxin IV

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33
Q

What is the best treatment for acidosis?

A

sodium bicarb IV, 1/6 molar sodium lactate, lactated ringers

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34
Q

What is the best treatment for alkalosis?

A

normal saline IV followed by ammonium chloride PO

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35
Q

What is the best treatment for pain?

A

opioids (fentanyl)

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36
Q

What is the best treatment for CNS depression?

A

artificial respiration

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37
Q

What is the best treatment for CNS stimulation?

A

anticonvulsants - diazepam, propoflo, phenobarb

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38
Q

When are emetics used?

A

within 1-2 hours of ingestion of the poison

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39
Q

What are contraindications of emetics?

A

unconsciousness, corrosives (bleach), petroleum products, dehydration, convulsions

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40
Q

What is the DOC for emesis in the dog?

A

apomorphine

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41
Q

What is the antidote for apomorphine?

A

naloxone IV of levallorphan

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42
Q

What is the DOC for emesis in cats?

A

xylazine

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43
Q

What are some other choices of emetics?

A

syrup of epilac, fresh ground mustard, saturated solution of sodium chloride, hydrogen peroxide

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44
Q

What is gastric lavage?

A

in unconscious ar anesthetized animals, use stomach or ET tube and flush with water and activated charcoal

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45
Q

What is enterogastric lavage?

A

combination of stomach tube and enema

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46
Q

What are the purgatives?

A

sodium sulfate, magnesium sulfate, mineral oil

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47
Q

What is used for precipitation?

A

chemicals that bind the toxicant

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48
Q

What is the precipitant for lead?

A

sulfate

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49
Q

What is the precipitant for oxalate?

A

calcium

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50
Q

What is the precipitant for alkaloids?

A

tannic acid

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51
Q

What is the adsorbent of choice?

A

activated charcoal

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52
Q

What kind of charcoal is most effective?

A

plant in small particle size

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53
Q

What is charcoal NOT effective for?

A

ethanol, methanol, heavy metal salts, fuoride, iodides, nitrate,nitrite, sodium chloride, bleach, fertilizer

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54
Q

What drug decreases the effectiveness of charcoal?

A

ipecac

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55
Q

What are the most commonly used diuretics?

A

mannitol (safer) and furosemide

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56
Q

What must be monitored before using diuretics and fluids to enhance elimination?

A

ensure renal function and hydration of animal

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57
Q

What are examples of urinary acidifiers?

A

ammonium chloride, methionine

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58
Q

What do urinary acidifiers help excrete?

A

weak basic drugs ex: alkaloids, amphetamines

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59
Q

What are examples of urinary alkalinizes?

A

sodium bicarbonate

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60
Q

What do urinary alkalinizes help excrete?

A

weak acidic drugs ex: NSAIDS, phenobarb

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61
Q

kg > lb

A

1 kg = 2.2 lb

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62
Q

gal > L > mL

A

1gal = 4L = 4000mL

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63
Q

qt > L > mL > oz

A

1qt = 1L = 1000mL = 32oz

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64
Q

pt > mL > oz

A

1pt = 500mL = 16oz

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65
Q

oz > g

A

1oz = 30g

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66
Q

fl oz > mL

A

1 fl oz = 30mL

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67
Q

gr > mg

A

1gr = 65 or 60mg

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68
Q

m > drop

A

1m = 1 drop

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69
Q

cup > mL > oz

A

1 cup = 250mL = 8oz

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70
Q

T > t > mL

A

1T = 3t = 15mL

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71
Q

t > mL

A

1t = 5mL

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72
Q

What are the organophosphates?

A

names that have derivatives of word “phosphorus”

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73
Q

What is the source of organophosphates?

A

empty pesticide containers, spraying of infectious agents, contaminated feed or drinking water

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74
Q

What is the difference between organophosphates with direct AChE and those without?

A

those without must be desulfurated before becoming active

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75
Q

How long do organophosphates persist in the environment?

A

not long 2-4 weeks, can penetrate waxy coatings or skin and live longer

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76
Q

What is storage activation of organophosphates?

A

become active and more toxic if sealed and stored 1-2years

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77
Q

What are the toxicokinetics of organophosphates?

A

lipophillic, crosses membranes easily, can absorb through skin or GI or inhaled, well distributed throughout body, enters CNS, no tissue accumulation, tolerance

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78
Q

Which organophosphate is more lipophilic and can sequester in fat and stay in body longer?

A

dichlorvos

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79
Q

What is lethal synthesis?

A

when metabolites are more toxic than original compound

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80
Q

Which age of animals are less effected by lethal synthesis?

A

young animals

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81
Q

What is the MOA of organophosphates?

A

irreversible inhibition of cholinesterase’s - non-competitive - increases ACh at all cholinergic sites

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82
Q

What is the cause of death in high exposure of organophsphates?

A

respiratory failure (paralysis), delayed neurotoxicity

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83
Q

What is the onset of action for organophosphates?

A

rapid 15mins - 1hour

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84
Q

What are the acute clinical sigs of organophosphate toxicity?

A

muscarinic stimulation, nicotinic stimulation, CNS stimulation, nicotinic blockade > paralysis, coma, dyspnea, death

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85
Q

What is organophosphate induced intermediate syndrome?

A

with massive doses (malicious) don’t see the initial muscarinic signs and jump right to nicotinic and CNS stimulation

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86
Q

What is organophosphate induced delayed polyneuropathy?

A

peripheral neurotoxicity after surviving acute poisoning - see muscle weakness, ataxia, 10-14 days after exposure

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87
Q

What is seen on pathology in organophosphate toxicity?

A

nonspecific lesions - pulmonary edema, hemorrhage, necrosis of skeletal muscle, pancreatitis

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88
Q

How do you test for organophosphates?

A

stomach/rumen contents, skin from dermal exposure NOT liver/kidney because metabolism is rapid - or look at ACh activity in blood

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89
Q

How do you diagnose organophosphate toxicity?

A

history of exposure, clinical signs, +/- lab testing, atropine response test (if strong response, probably NOT OP)

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90
Q

What are the DDX for organophosphate poisoning?

A

pyrethrins, tremorgenic mycotoxins, amitraz toxicosis, blue-green algae, muscarinic mushrooms

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91
Q

How do you treat organophosphate toxicity?

A

induce emesis (NOT if depressed or seizures), wash with soap water, activated charcoal, supportive care

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92
Q

What should be avoided when treating for organophosphate toxicity?

A

phenothiazines, aminoglycosides, muscle relaxants, drugs that depress respiration (opioids)

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93
Q

What drugs are used for organophosphate toxicity?

A

atropine, 2-PAM

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94
Q

What is the antidote for OP toxicity?

A

2-PAM, pralidoxime, protopam - may not be effective if aging has occurred or against all OP

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95
Q

How do you treat intermediate syndrome in OP?

A

supportive care, 2-PAM, may last for weeks

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96
Q

How do you treat OP-induced delayed polyneuropathy?

A

symptomatic therapy only

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97
Q

What is the prognosis for organophosphate toxicity?

A

lots of factors, mild to moderate generally treatable, acute cases responding to treatment can recover w.i 24 hrs

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98
Q

What are the carbamates?

A

names contain ‘carb’

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99
Q

Do carbamates undergo storage activation?

A

NO

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100
Q

What are the pharmacokinetics of carbamates?

A

does NOT require hepatic bioactivation, more toxic in young patients, fast onset, short duration, low exposure can recover w/o tx, metabolized rapidly

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101
Q

What is the MOA of carbamates?

A

reversible inhibition of acetylcholinesterase

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102
Q

When does toxicity occur in carbamates?

A

when carbamylation&raquo_space; hydrolysis

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103
Q

How do you diagnose carbamate toxicity?

A

measure cholinesterase levels but can give false results since reversible, also not detectable in tissues, blood secretions due to rapid metabolism

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104
Q

What is the treatment for carbamates?

A

atropine, 2-PAM although not reliable

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105
Q

In what carbamate is 2-PAM contraindicated?

A

carbaryl, can increase carbamylation process

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106
Q

What are the chlorinated hydrocarbons (organochlorines)?

A

diphenol aliphatics, aryl hydrocarbons, cyclodienes

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107
Q

When were chlorinated hydrocarbons started?

A

DDT to control disease vectors, lindane for lice in humans

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108
Q

Are chlorinated hydrocarbons lipophillic or non-lipophillic?

A

HIGHLY lipophillic –> bioaccumulation in food chain, residues in tissues, persistent in environment

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109
Q

How long do chlorinated hydrocarbons live in the environment?

A

2-15YEARS

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110
Q

What is the toxicity of chlorinated hydrocarbons like?

A

low toxicity to mammals, cats most sensitive but all animals susceptible

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111
Q

How are chlorinated hydrocarbons absorbed?

A

readily absorbed, distributed everywhere

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112
Q

How are chlorinated hydrocarbons excreted?

A

milk, feces, urine, bile (can be reabsorbed)

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113
Q

How does fat effect the TK of chlorinated hydrocarbons?

A

acts as a sink, keeps it then redistributes after weeks, months - weight loss can disrupt equilibrium

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114
Q

Because of the biliary excretion, what is a good treatment for chlorinated hydrocarbons?

A

activated charcoal

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115
Q

What is the MOA of chlorinated hydrocarbons?

A

Na influx and K efflux in peripheral nerves > partial depolarization of brain> repetitive firing of neuron > axonal hyperactivity

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116
Q

What are the clinical signs of chlorinated hydrocarbon toxicity?

A

CNS stimulation, repetitive firing, weakness, tremors, spastic gait, seizures

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117
Q

What species shows different clinical signs of chlorinated hydrocarbon toxicity?

A

birds show CNS depression and blindness

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118
Q

How do you diagnose chlorinated hydrocarbon toxicity?

A

chemical analysis find in liver, blood or brain in high concentrations - high in fat is not conclusive, no pathognomotic lesions

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119
Q

What is the antidote for chlorinated hydrocarbons?

A

NONE

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120
Q

How do you treat chlorinated hydrocarbon toxicity?

A

emesis, wash with soap, activated charcoal, IV lipid therapy, diazepam for seizures, oxygen, fluids

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121
Q

What is the concern about chlorinated hydrocarbons in wildlife?

A

bioaccumulation and biomagnification, embryo toxicity, thinning eggshells, toxic to aquatics

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122
Q

What are pyrethrins?

A

extract from flowers - chrysanthemums, also used as an insecticide

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123
Q

What are pyrethroids

A

synthetic analog of pyrethrins

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124
Q

How long do pyrethrins last in the environment?

A

NOT long, unstable in air and light

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125
Q

What is different between the 1st and 2nd generation pyrethroids?

A

gen 1 do NOT have alpha-cyano moiety = less potent

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126
Q

What is the toxicity of pyrethrins like to mammals?

A

low, no subacute or chronic forms

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127
Q

What species are pyrethrins very toxic to?

A

fish and some birds - cats more than dogs

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128
Q

Are pyrethrins lipid soluble or non-lipid soluble?

A

lipid soluble

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129
Q

Where are pyrethrins metabolized?

A

GIT, plasma and liver - RAPIDLY

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130
Q

Do pyrethrins accumulate in tissues?

A

NO - no residual effect

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131
Q

How does piperonyl but oxide effect pyrethrins?

A

inhibits metabolism

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132
Q

What is the MOA of pyrethrins?

A

delay closure of Na ion channels in axonal membrane of insect, inhibits ATPase leads to repetitive firing

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133
Q

What is the knockdown effect?

A

rapid paralysis caused by inhibition of neurons -> insect immobile but not dead

134
Q

What type of pyrethroids have a greater effect?

135
Q

Why do pyrethroids effect insects more than mammals?

A

work better at lower temp, insect Na channels more sensitive and recover slower, insects have slower metabolism

136
Q

What are some clinical signs of pyrethrin toxicity?

A

muscle tremors, fine tremors instead of convulsions, depression, ataxia, GI signs, dyspnea, death

137
Q

How do you diagnose pyrethrins?

A

no specific lesions, toxins ID in liver and brain, clinical signs with history

138
Q

What is the antidote for pyrethrins?

139
Q

How do you treat pyrethrin toxicity?

A

wash off, control temp - NO activated charcoal or phenothiazines, treat symptoms, IV lipid therapy

140
Q

What drug can be given to control muscle tremors in pyrethrin toxicity?

A

methocarbamol

141
Q

What can help control seizures in pyrethrin toxicity?

A

diazepam, barbituates, propofol

142
Q

Where did rotenone come from?

A

roots of tropical plants, used for fishing to kill fish

143
Q

What is rotenone in?

A

insecticides, home garden supplies, flea/tick treatment, pesticide for chickens, dust on crops

144
Q

What species is rotenone very toxic to?

A

fish and cold blooded animals - converted to highly toxic metabolites that are absorbed in gills

145
Q

Which mammals are most sensitive to rotenone?

A

pigs - most mammals converted to non-toxic metabolites

146
Q

What is the absorption of rotenone like?

A

low and incomplete through GI, inhalation more toxic - fats and oils increase absorption

147
Q

How is rotenone eliminated?

A

w/i 24hrs in the feces

148
Q

What is the MOA of rotenone?

A

blocks TCA cycle - therefore blocks production of ATP, free radical formation, also anesthetic effect with nerve axons

149
Q

What are the clinical signs of rotenone toxicity?

A

local irritation, depression, convulsions

150
Q

How do you test for rotenone?

A

look for compound in stomach contents, feces, urine, history

151
Q

How do you treat rotenone toxicity?

A

no treatment - supportive tx

152
Q

What are the sources of D-Limonene?

A

OTC lice, flea, tick products, essential oil, food fragrant

153
Q

What is the toxicity of D-Limonene like?

A

dogs and cats susceptible, cats > dogs

154
Q

How well is D-Limonene absorbed?

A

lipid soluble - readily absorbed through GI and skin, wide distribution

155
Q

What are the clinical signs of D-Limonene toxicity?

A

ataxia, weakness, paralysis, CNS depression, smell like lemons

156
Q

How do you diagnose D-Limonene toxicity?

A

exposure history

157
Q

How do you treat D-Liminene toxicity?

A

wash out, monitor temperature

158
Q

Where does nicotine come from?

A

alkaloid from dried leaves of nicotiana tabacum, nicotine sulfate is also a plant insecticide

159
Q

What is the LD50 of nicotine in dogs?

A

9.2mg - most nicotine products (cigarettes, cigars, patches etc) have a lot above that

160
Q

How well is nicotine absorbed?

A

well by inhalation and skin contact but poorly from ingestion unless stomach is alkaline

161
Q

How is nicotine excreted?

A

bile and urine

162
Q

What is the MOA of nicotine?

A

mimics ACh and stimulates post-synaptic nicotinic receptors, stimulates CRTZ, can block at high doses

163
Q

What are some clinical signs of nicotine toxicity?

A

ataxia, hypersalivation, bradycardia, tremors, CNS depression, paralysis of reps muscles > death

164
Q

How do you diagnose nicotine poisoning?

A

contents in urine, stomach, kidney, liver, blood - history

165
Q

How do you treat nicotine toxicity?

A

emesis, activated charcoal, acidify urine, fluids, NO antacids, atropine, control seizures

166
Q

What drug is a nonselective nicotinic antagonist used to curb tobacco addiction in humans?

A

mecamylamine

167
Q

What is amitraz used for?

A

preventic collars, swine insecticide, plant insecticide

168
Q

What species are amitraz products contraindicated in?

A

cats and horses

169
Q

What is the acute oral LD50 of amitraz for dogs?

A

100-150mg/kg

170
Q

What can increase the toxicity of amitraz?

A

meperidine, sympathomimetic amines, stress

171
Q

How is amitraz absorbed?

A

PO, inhalation, skin

172
Q

What is the distribution of amitraz?

A

throughout body including CNS

173
Q

What is the MOA of amitraz?

A

A2 adrenergic agonist in CNS, A1 and A2 adrenergic agonist in the ANS, MAO inhibitor

174
Q

What are the clinical signs of amitraz toxicity?

A

bradycardia, ataxia, CNS depression, hypothermia, V/D, cardiovascular collapse, respiratory failure

175
Q

How do you diagnose amitraz toxicity?

A

chemical analysis of organs, hyperglycemia, history, clinical signs

176
Q

What are the DDX for amitraz toxicity?

A

cholinesterase inhibitors, pyrethrins

177
Q

What is the antidote for amitraz toxicity?

A

A2 antagonists: yohimbine, atipamezole

178
Q

What are the treatment methods for amitraz toxicity?

A

washing, emesis, activated charcoal, cathartics, supportive care, antidote

179
Q

What is DEET used for?

A

insect repellant for mosquitos, flies and ticks

180
Q

What species are susceptible to DEET toxicity?

A

cats > dogs, young animals more sensitive

181
Q

How is DEET absorbed?

A

in skin, accumulates and persists

182
Q

What is the MOA of DEET?

A

unknown but causes surface irritation

183
Q

What are the clinical signs of DEET toxicity?

A

depression or excitation, ataxia, tremors, seizurees, hypersalivation, vomiting

184
Q

How do you diagnose DEET toxicity?

A

20ppm findings in body contents, history, clinical presentation

185
Q

What is the antidote for DEET toxicity?

186
Q

How do you treat DEET toxicity?

A

wash, emesis, activated charcoal, treat symptoms

187
Q

What is naphthalene found in?

A

mothballs, organochlorine insecticide

188
Q

What species are susceptible to naphthalene toxicity?

A

cats > dogs

189
Q

How is naphthalene absorbed?

A

PO, inhalation and oils from skin can absorb

190
Q

What is the MOA of naphthalene?

A

irritant, oxidation products cause methemoglobinemia and hemolysis > tissue hypoxia

191
Q

What are the clinical signs of naphthalene toxicity?

A

mothball breath, salivation, vomiting, diarrhea, hemolysis, heinz bodies, methemoglobinemia, seizures

192
Q

How do you diagnose naphthalene toxicity?

A

hematologic changes - must differentiate from other causes of RBC oxidative injury, measure levels in blood

193
Q

What is the treatment for naphthalene?

A

ascorbic acid, methylene blue - emesis, sodium bicarb, supportive care

194
Q

What is ivermectin in?

A

a macrocytic lactone, endectocide for heartworm and other parasites

195
Q

What species are prone to ivermectin toxicity?

A

dogs, small birds, collies especially

196
Q

How is ivermectin absorbed?

A

PO and excreted unchanged in feces

197
Q

What is the half life of ivermectin?

A

2 days - go with 5x that to get out of system!

198
Q

What is the MDR1 gene mutation?

A

lack of the MDR1 gene > 50x concentration of drug in the CNS

199
Q

What is the MOA of ivermectin?

A

GABA agonist

200
Q

What are the clinical signs of ivermectin toxicity?

A

CNS depression, ataxia, hypersalivation, coma,

201
Q

How do you diagnose ivermectin toxicity?

A

chemical analysis, history, clinical presentation

202
Q

What is the antidote for ivermectin?

203
Q

How do you treat ivermectin toxicity?

A

emesis, activated charcoal, picrotoxin, physostigmine, supportive care

204
Q

What are the 1st generation anticoagulant rodenticides?

A

warfarin, pindone, chlorophacinone

205
Q

What are the second generation anticoagulant rodenticides?

A

brodifacoum, diphacinone, bromodialone

206
Q

What are the second generation anticoagulant rodenticides used for?

A

pesticides, baits, powders mixed with food maliciously, eating rats/mice that ingested toxic compounds

207
Q

What is secondary toxicosis AKA relay toxicosis?

A

rat dies from toxin, cat eats rat and is effected by toxin

208
Q

How long do anticoagulant rodenticides last in the environment?

A

resistant, last weeks to months

209
Q

What are some properties of anticoagulant rodenticides?

A

odorless and tasteless, action is slow

210
Q

Which generation of anticoagulant is more toxic?

A

2nd gen effective after one dose, 1st gen more toxic when ingested daily for a week

211
Q

What species are susceptible to anticoagulant rodenticides?

A

most - pigs, dogs, cats, ruminants, horse, chickens

212
Q

What can enhance toxicosis of anticoagulant rodenticides?

A

vit K deficiency, liver dz, enzyme inhibitors, drugs that cause hemorrhage, anemia, etc, steroids or thyroxine

213
Q

What decreases toxicity of anticoagulant rodenticides?

A

pregnancy, lactation, enzyme inducers

214
Q

When do anticoagulant rodenticides reach peak values?

215
Q

Are anticoagulant rodenticides protein bound?

A

yes, highly bound

216
Q

What is the DOA of anticoagulant rodenticides?

A

3-4 weeks, long half life

217
Q

Do anticoagulant rodenticides get in milk?

A

yes, also cross placenta

218
Q

What is the MOA of anticoagulant rodenticides?

A

inhibit vit K epoxide reductase, depletes reduced vit K, reduced activation of clotting factors 2,7,9,10

219
Q

When is the onset of clinical signs for anticoagulant rodenticides?

220
Q

What are the clinical signs for anticoagulant rodenticide poisoning?

A

tachypnea, dyspnea, anemia, anorexia, lethargy, hemorrhage, abortion in cattle, death without external evidence of bleeding

221
Q

What are the pathologic lesions associated with anticoagulant rodenticide toxicity?

A

bleeding, petechiation, bacterial pneumonia

222
Q

What is the chemical analysis for rodenticide toxicity?

A

detection in blood, coagulation parameters

223
Q

Which test is the earliest indicator of rodenticide toxicity?

A

PIVKA (sent to lab)

224
Q

What is the treatment for anticoagulant rodenticides?

A

RBC, FFP, fluids, oxygen, thoracocentesis -

225
Q

How do you know if you need to treat anticoagulant rodenticides with FFP or whole blood?

A

check PCV <15 give blood

226
Q

What drug is used to treat anticoagulant rodenticide toxicity?

A

vit K1 PO, bioavailability better after fatty meal, (IV=anaphylaxis, IM=hemmorrhage) won’t work for 24 hours, animals in liver failure may not respond

227
Q

Which type of vitamin K is used for anticoagulant rodenticide treatment?

228
Q

When should you recheck the PT in rodenticide poisoning?

A

Not treating - 36hr and 96hr

treating - 36hr and 48hr

229
Q

Whats is cholecalciferol used in?

A

rodenticides, bait, large does of bit D, poisonous plants, human meds/vitamins

230
Q

Which vitamin is CCF?

231
Q

What is the solubility of CCF?

A

insoluble in H20, soluble in most organic solvent and oil

232
Q

What species are more susceptible to CCF poisoning?

A

all, young more sensitive

233
Q

Is vit D toxicity acute or chronic?

A

can be either depending on preparation

234
Q

What are some predisposing factors for CCF toxicity?

A

renal disease, hyperparathyroid, ingestion of lots of calcium and phosphorus

235
Q

What happens to CCF in the body?

A

absorbed by GI, binds to serum vitD binding protein, to liver, metabolized to 25 hydroxycholecalciferol (calcidiol) brought to kidney > 1,25 dihydroxycholecalciferol (calcitriol)

236
Q

How is CCF excreted?

A

bile, feces, milk (toxic levels)

237
Q

What is the MOA of CCF?

A

increases serum calcium due to increased GI absorption, hyperphosphatemia, deposits calcium in soft tissues

238
Q

What effects does CCF toxicity have?

A

tissue damage, increased capillary permeability, hemorrhage, loss of sodium and potassium

239
Q

When do clinical signs of CCF toxicity happen?

A

24-36 hours

240
Q

What are the clinical signs of CCF toxicity?

A

depends on tissues affected - PU/PD, arrhythmias, vomiting, abdominal pain, muscle twitching, seizures, coma, death

241
Q

What is the main lesion associated with CCF toxicity?

A

hemorrhagic gastroenteritis

242
Q

What does the lab work look like of an animal with CCF toxicity?

A

hypercalcemia, hyperphosphatemia, elevated serum 25 hydroxy and 1,25 dihydroxycholecalciferol, decreased iPTH

243
Q

How do you diagnose CCF toxicity?

A

history, clinical signs, lab, calcification of tissues

244
Q

How do you treat CCF toxicity?

A

emetics, activated charcoal, saline cathartic, normal saline, furosemide, glucocorticoids, calcitonin, pamidronate disodium, low Ca diet, stay out of sun

245
Q

Where does bromethalin come from?

A

general use pesticide, bait

246
Q

What animals are sensitive to bromethalin toxicity?

A

cats > dogs, g-pigs are resistant!

247
Q

How is bromethalin absorbed and distributed?

A

hgihly lipophilic, absorbed PO, widely distributed, highest in brain and fat

248
Q

What is bromethalin metabolized to?

A

more toxic metabolite desmethylbromethalin in liver

249
Q

How is bromethalin excreted and what is the half life?

A

5-6 days, in bile, urine

250
Q

What is the MOA of bromethalin?

A

uncoupling of oxidative phosphorylation, lack of adequate ATP, insufficient energy for Na/K ion pumps, cerebral and spinal cord edema

251
Q

Which part of the body is the main target in bromethalin poisoning?

252
Q

When do signs of toxicity occur with bromethalin?

A

acutely 2-24hrs, subacute 2-3 days

253
Q

What are the clinical signs of bromethalin toxicity?

A

muscle tremors, hyperthermia, seizures, ataxia, paralysis, hyperreflexia, UMN bladder

254
Q

What lesions are found in bromethalin toxicity?

A

cerebral edema, diffuse white matter vacuolization in CNS

255
Q

How do you diagnose bromethalin toxicity?

A

history, clinical signs, brain imaging of white matter vacuolization in CNS, chemical analysis TAT 5-7days

256
Q

What is the antidote for bromethalin toxicity?

257
Q

How do you treat bromethalin toxicity?

A

emetic, activated charcoal, saline cathartic, mannitol, diazepam, supplemental feeding

258
Q

What is strychnine in?

A

restricted use pesticide to control gophers and squirrels, ingest bait or relay toxicosis

259
Q

What does strychnine come from?

A

strychnos seeds, bitter taste, poorly water soluble, white powder

260
Q

How long does strychnine live in the environment?

A

gone from soil w/i 40 days

261
Q

What species are susceptible to strychnine toxicity?

A

dogs, horses, cattle, pigs > cats

262
Q

What species are resistant to strychnine toxicity?

263
Q

What can decrease toxicity of strychnine?

A

committing, food in stomach, small amt over time

264
Q

How is strychnine absorbed?

A

from GI > crosses BBB > liver

265
Q

How is strychnine eliminated?

266
Q

Is strychnine PP bound?

267
Q

How soon is strychnine eliminated?

A

w/i 24 hours

268
Q

What is the MOA of strychnine??

A

blocks postsynaptic effect of inhibitory glycine in spinal cord leading to highly exaggerated reflex arcs

269
Q

When is the onset of strychnine toxicity?

A

15min - 2hr, rapid death

270
Q

What are the clinical signs of strychnine poisoning?

A

panting, vomiting, mydriasis, stiffness, muscle twitches, seizures, death by respiratory failure

271
Q

What lab samples can be tested for strychnine poisoning?

A

urine, stomach contents, liver

272
Q

How do you diagnose strychnine toxicity?

A

history, clinical signs, lab

273
Q

How do you treat strychnine toxicity?

A

apomorphine for emesis, gastric lavage, activated charcoal, symptomatic treatment

274
Q

What is contraindicated in the lavage for strychnine toxicity?

A

sodium bicarbonate, antacids

275
Q

What drugs are used for symptomatic treatments of strychnine poisoning?

A

pentobarbitol, diazepam, methocarbamol, guaifenesin, xylazine

276
Q

What is zinc phosphate used for?

A

restricted use pesticides, phosphine gas, baits, poisoned rodents

277
Q

Is zinc phosphate stable in the environment?

A

stable when dry, decomposes on air or bait w/i 2 weeks, insoluble in H20

278
Q

What type of zinc phosphide leads to acute toxicity?

A

acute from phosphine gas, chronic from either phosphine gas OR zinc phosphide

279
Q

What enhances zinc phosphide toxicity?

A

gastric acid - causes hydrolysis of zinc phosphide to phosphine gas at pH 4 or lower

280
Q

How are zinc phosphides absorbed?

A

in GI tract and inhalation, - GI irritant (skin insignificant)

281
Q

how is absorbed phosphine excreted?

A

lungs , urine

282
Q

What is the MOA of zinc phosphide?

A

unknown - increases oxygen radicals and direct GI irritation, damage to blood vessels

283
Q

What are the main tissues affected by zinc phosphide toxicity?

A

brain, heart, kidney, liver, lung

284
Q

What are the clinical signs of zinc phosphide toxicity?

A

anorexia, vomiting, increased rate and depth of respiration, abdominal pain, bloat, dyspnea, death, CNS stimulation in dogs, yelping and convulsions

285
Q

What is the onset like of zinc phosphide?

A

rapid - mins to hours

286
Q

Why does death occur in zine phosphide toxicity?

A

tissue anoxia

287
Q

What are the classic lesions of zinc phosphide toxicity?

A

odor of rotten fish/garlic, hemorrhagic gastroenteritis, congestion of liver and kidney, pulmonary edema

288
Q

What does the lab work show in zinc phosphide toxicity?

A

elevated serum zinc, metabolic acidosis

289
Q

How should specimens of zinc phosphide toxicity be contained to send to lab?

A

rapidly frozen

290
Q

How do you diagnose zinc phosphide toxicity?

A

history, acetylene odor, clinical signs, rapid onset/death, lab diagnosis

291
Q

Does zinc phosphide pose a risk to hospital staff?

A

YES! if smelling it at 2ppm (safe limit is 1ppm)

292
Q

What is the antidote for zinc phosphide toxicity?

293
Q

What is the treatment for zinc phosphide?

A

emetics, gastric lavage, PO antacids, activated charcoal, IV fluids, O2, circulatory and pulmonary support,

294
Q

Where does fluoroacetate come from?

A

called compound 1080, used to control coyotes, and rodents, collar worn by sheep and goats

295
Q

How do animals get fluoroacetate poisoning?

A

eating poisoned rodents, eating plants that contain fluoroacetate

296
Q

Doe fluoroacetate survive long in the environment?

A

chemically stable but degraded by soil microorganisms and plant enzymes, odorless and water soluble but insoluble in most organic solvents

297
Q

What species are effected by fluoroacetate toxicity?

A

dogs > mammals

298
Q

How is fluoroacetate absorbed?

A

GI tract, lungs, open wounds but NOT intact skin

299
Q

How is fluoroacetate excreted?

300
Q

What is the MOA of fluoroacetate?

A

condenses w/ oxaloacetate and competes w citrate for active site of CAC - slows the CAC, decreases respiration and energy, buildup of citrate

301
Q

Which organs are most effected by fluoroacetate toxicity?

A

brain (ammonia buildup) and heart

302
Q

What are the clinical signs of fluoroacetate toxicity?

A

rapid onset of GI hyperactivity, CNS stimulation, hyperthermia, heart failure, colic, convulsions

303
Q

What lesions are associated with fluoroacetate toxicity?

A

rapid rigor mortis, cyanosis, hemorrhages, pulmonary changes, organ congestion

304
Q

What does the lab work show in fluoroacetate toxicity?

A

elevated citrate, hyperglycemia, metabolic acidosis, ionized hypocalcemia

305
Q

How do you diagnose fluoroacetate toxicity?

A

history, clinical signs, lesions

306
Q

How do you treat fluoroacetate toxicity?

A

activated charcoal, with rapid onset tx may not be an option

307
Q

What is the antidote for fluoroacetate toxicity?

308
Q

What drugs can be given in fluoroacetate poisoning?

A

calcium chloride for ventricular arrhythmias, sodium bicarb for metabolic acidosis, oxygen, fluids

309
Q

How do animals get water deprivation?

A

feedining brine, whey or garbage, ingestion of salt licks, drinking water containing salt, overcrowding, frozen water, lack of water, medicated (unpalatable) water

310
Q

What effect does salt have on animals?

A

taste is attractive, mild irritant to mucous membranes

311
Q

How much salt can animals tolerate in feed?

A

> 10% salt in feed if they have free access to water

312
Q

What species are susceptible to water deprivation?

A

pigs, cattle and poultry mostly, dogs less

313
Q

How is salt absorbed?

A

by GI and distributed all over body - enters brain by passive diffusion and removed by active transport

314
Q

How is excess sodium excreted?

A

in urine, as long as there is enough water

315
Q

What is the MOA of water deprivation?

A

dehydration increases plasma sodium and cerebral spinal fluid - high sodium in brain inhibits anaerobic glycolysis resulting in lack of energy for active transport

316
Q

What happens with sodium trapped in the brain?

A

attracts water because of osmotic gradient > cerebral edema and brain damage

317
Q

What are the clinical signs of water deprivation?

A

early constipation and thirst, vomiting, PU, metabolic acidosis, seizures, circling, head pressing, blindness

318
Q

What lesions are seen in water deprivation that are pathognomonic?

A

eosinophilic meningoencephalitis is pathognomonic in PIGS ONLY and only within 24 hours of exposure - disappears after

319
Q

What other lesions could be seen with water deprivation?

A

fluid in body cavities, organ edema, cerebral edema

320
Q

What is used for lab diagnosis of water deprivation?

A

serum and CSF concentrations, salt in feed

321
Q

How do you diagnose water deprivation?

A

history, encephalitic signs, lesions and lab diagnosis

322
Q

How do you treat water deprivation?

A

give small amounts of fresh water - large amount can kill them by causing more cerebral edema, IV fluids, furosemide, anticonvulsants

323
Q

What is the prognosis of water deprivation?

A

poor, mortality 50%

324
Q

What is the source of acute copper toxicosis?

A

ingestion of high concentrations of copper - feed additives, in soil

325
Q

Why is acute heavy metal toxicity bad?

A

very small amount can cause toxicosis, irritants, poor penetrated of membranes, small amount that is absorbed can cause toxicosis because of potency

326
Q

Which heavy metal crosses the BBB and causes CNS damage?

327
Q

What are the clinical signs of acute copper toxicosis?

A

rapid onset of GI signs, dehydration, shock

328
Q

What species is chronic copper poisoning common in?

A

sheep > cattle, due to lower maliptinum in sheep that enhance copper toxicosis

329
Q

What is the treatment for acute copper toxicosis?

A

supportive and symptomatic therapy

330
Q

What enhances excess copper in the body?

A

molybdenum deficiency

Toxicology (4 decks)

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