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ZUKU NAVLE PREP > Cross Species - Top 20 Toxicosis Part 4 > Flashcards

Cross Species - Top 20 Toxicosis Part 4 Flashcards

1
Q

what animals are most often affected by toad toxicity?

A

dogs affected most - sometimes cats

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2
Q

what body systems are affected by toad toxicity?

A

CNS, cardiovascular system

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3
Q

what are the toxic principles in toad toxicity?

A

bufagenins - act like digitalis, bufotoxins - act like local anesthetics, catecholamines, serotonin (block sodium channels in nerves)

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4
Q

what is the most toxic toad found in the us?

A

giant or marine toad (rhinella marina) - florida, texas, & hawaii

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5
Q

how is toad toxicity diagnosed?

A

history of exposure

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6
Q

how is toad toxicity treated?

A

thoroughly rinse mouth, treat any cardiac arrhythmias & give digoxin specific antibody If refractory, decrease salivation (atropine if normal cardiac rhythm), benzos for CNS excitement, & oxygen therapy for cyanosis

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7
Q

when is toad toxicity most often seen?

A

warm weather

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8
Q

what clinical signs are seen with toad toxicity?

A

oral irritation/frothing/pawing at mouth, retching, vomiting, cyanosis, cardiac arrhythmias, seizures, & death

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9
Q

what are the major categories of insecticides that commonly cause toxicosis?

A

organophosphates, carbamates, organocholines, & pyrethrins

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10
Q

what body systems are affected by organophosphates & carbamates?

A

all systems - especially gi, neuromuscular, & CNS

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11
Q

what muscarinic clinical signs are seen with insecticide toxicity?

A

SLUD - salivation, lacrimation, urination, & diarrhea

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12
Q

what nicotinic clinical signs are seen with insecticide toxicity?

A

muscle tremors & weakness

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13
Q

what central nervous system clinical signs are seen with insecticide toxicity?

A

anxiety, ataxia, & seizures

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14
Q

what body system is affected by organochlorines?

A

CNS

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15
Q

what clinical signs are seen with organochlorine toxicity?

A

abnormal behavior, posture, vocalization, neuromuscular tremors, convulsions, & hyperthermia

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16
Q

what body system is affected by pyrethrin toxicity?

A

CNS

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17
Q

what clinical signs are seen with pyrethrin toxicity?

A

tremors, seizures, incoordination, hunched back, salivation, & death

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18
Q

how is organophosphate toxicosis diagnosed?

A

measure acetylcholinesterase concentration in blood & brain (usually a 70% or more decrease) & measure organophosphates in stomach/rumen, blood/serum, & urine

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19
Q

how is carbamate toxicosis diagnosed?

A

measure acetylcholinestersae concentration in blood/brain (usually 50% or more decrease) & measure carbamates in stomach/rumen, blood/serum, urine

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20
Q

how is organochlorine toxicosis diagnosed?

A

measure organochlorines in brain/liver/kidney/fat/stomach & check blood/urine in rest of herd/flock

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21
Q

how is pyrethrin toxicosis diagnosed?

A

measure pyrethrins/pyrethroids in tissues/fluids

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22
Q

what treatment is used for organophosphate toxicity?

A

decontamination, atropine, 2-PAM, & diazepam for seizures

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23
Q

what drug class should not be given to an animal with organophosphate toxicosis?

A

phenothiazines - will potentiate organophosphate

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24
Q

what treatment is used for carbamate toxicity?

A

decontamination, atropine, no 2-PAM!!!

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25
Q

why can 2-PAM not be used in an animal with carbamate toxicity?

A

can reversibly bind & inhibit acetylcholinestersae & may exacerbate clinical signs

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26
Q

what treatment is used for organochlorine toxicity?

A

bathe if dermal exposure, decontamination, reduce stress, barbiturates, or diazepam

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27
Q

what treatment is used for pyrethrin toxicity?

A

bathe if dermal exposure, activated charcoal, barbiturates, or diazepam

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28
Q

why not induce emesis for a case of pyrethrin toxicity?

A

petroleum solvent may cause aspiration pneumonia

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29
Q

what is the pathophysiology of organophosphate toxicity?

A

irreversibly inactivates acetylecholinesterase at synapses & in erythrocytes

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30
Q

why are newer organophosphates considered to be safer?

A

they require hepatic activation

31
Q

what is the pathophysiology of carbamate toxicity?

A

reversibly inactivates acetylcholinesterase at synapses and in erythrocytes

32
Q

T/F: carbamates are considered to be safer than organophosphates and are used more often

A

TRUE

33
Q

why are organochlorines not frequently used?

A

tissue residues & chronic toxicity

34
Q

what is the pathophysiology of organochlorines?

A

CNS stimulation

35
Q

what is the pathophysiology of pyrethrin toxicity?

A

affect sodium, chloride, & calcium channels - affect nicotinic acetylcholine receptors

36
Q

where are pyrethrins & pyrethroids derived from?

A

pyrethrins: plant c. cinerariaefolium, pyrethroids: synthetic derivatives of pyrethrins

37
Q

what body systems are affected by petroleum product toxicity?

A

respiratory, gi, CNS, & dermal

38
Q

what animals are most often affected by petroleum product toxicity?

A

usually dogs, cats, or ruminants - all species are vulnerable

39
Q

what clinical signs are seen in all species with petroleum product toxicity?

A

excitability, incoordination, shivering, dyspnea, aspiration pneumonia, & death

40
Q

what clinical signs are seen in small animals with petroleum product toxicity?

A

salivation, cough, choking, & vomiting

41
Q

what clinical signs are seen in ruminants with petroleum product toxicity?

A

bloat

42
Q

what is the toxic principle of petroleum products?

A

volatile hydrocarbons

43
Q

how is petroleum product toxicity diagnosed?

A

odor of hydrocarbons from lungs/rumen contents/feces & measure hydrocarbons in lung/liver/kidney/gi contents

44
Q

what treatment is used for small animals with petroleum product toxicity?

A

activated charcoal and maybe antibiotics for pneumonia - do not induce emesis because of aspiration risk

45
Q

what treatment is used for ruminants with petroleum product toxicity?

A

relieve bloat with stomach tube

46
Q

what is the pathophysiology of petroleum product toxicity?

A

cns dysfunction - chemical aspiration pneumonia from low viscosity & high volatility (gasoline, kerosene) increase aspiration risk

47
Q

what is the prognosis for petroleum product toxicity that resulted in aspiration pneumonia?

A

poor

48
Q

when may animals be exposed to petroleum products causing toxicity?

A

dogs/cats may ingest when grooming & ruminants may ingest because curious or thirsty

49
Q

what animals are more severely affected by smoke inhalation?

A

smaller animals & birds

50
Q

when do clinical signs start & peak from smoke inhalation?

A

12-48 hours after inhalation & compromise peaks at 12-24 hours post-inhalation

51
Q

what clinical signs are seen from smoke inhalation?

A

coughing, stridor, tachypnea, dyspnea, voice change, depression, weakness, obtundation, & coma

52
Q

what are some examples of toxic principles from smoke inhalation?

A

carbon monoxide, cyanide gas, methane, sulfur trioxide, & pyrolysis products (cause polymer fume fever)

53
Q

what is the gold standard diagnostic for smoke inhalation?

A

laryngoscopy/bronchoscopy - see edema, ulceration, & subglottic injury

54
Q

is PaO2 affected by carbon monoxide poisoning?

A

nope

55
Q

how is smoke inhalation diagnosed?

A

pulse oximetry, arterial blood gas, elevated carboxyhemoglobin concentration, elevated lactate concentration, decreased PCV/hemoglobin (after 1 week)

56
Q

what may be seen on thoracic imaging on a smoke inhalation case?

A

atelectasis, pulmonary edema, hyperinflation at 24-36 hours post inhalation

57
Q

what may be seen on ecg on a case of smoke inhalation?

A

compatible with cariac ischemia (s-t segment elevation or depression & t wave inversion)

58
Q

what specific treatment is indicated for methemoglobinemia from smoke inhalation?

A

methylene blue

59
Q

what specific treatment is indicated for polymer fume fever?

A

acetylcysteine

60
Q

what treatment is used for smoke inhalation cases?

A

intubation or tracheostomy to administer oxygen, bronchodilators, antibiotics, & corticosteroids

61
Q

what is the pathophysiology of smoke inhalation?

A

thermal injury & inhaled toxicants

62
Q

T/F: steam produces SEVERE lung injury

A

TRUE

63
Q

what body system is affected by strychnine?

A

CNS

64
Q

what animals are most often affected by strychine?

A

all species are vulnerable but most often in western USA in young large breed intact male dogs

65
Q

what initial clinical signs are seen with strychnine toxicity?

A

nervous, stiff, & very rapid progression of clinical signs

66
Q

what clinical signs are seen from strychnine toxicity?

A

generalized rigidity, tetanic spasms, tonic clonic seizures, hyperthermia, & death

67
Q

what is the toxic principle of strychnine?

A

indole alkaloid

68
Q

how is strychnine toxicity diagnosed?

A

measure strychnine in stomach contents, liver, kidney, & urine

69
Q

how is strychnine toxicity treated?

A

decontamination, control seizures (pentobarb or methocarbamol), & prevent asphyxiation (intubate & breath for animal)

70
Q

where does strychnine come from?

A

seeds of indian tree strychnos nuxvomica

71
Q

what is the pathophysiology of strychnine toxicity?

A

competitive & reversible inhibition of the inhibitory neurotransmitter glycine at post-synaptic sites in spinal cord & medulla

72
Q

T/F: there is restricted use of strychnine in pesticides because it is so highly toxic

A

TRUE

73
Q

T/F: strychnine is often used in gopher bait

A

TRUE

ZUKU NAVLE PREP (178 decks)

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