Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Toxicology > Neurotoxicants > Flashcards

Neurotoxicants Flashcards

1
Q

what produces the most toxic compound on the planet?

A

Clostridium botulinum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ways to group clinical signs:

A

peripheral vs. central

excitatory vs. depressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

organophosphate pesticides

A
  • agricultural and residential use has increased since OCPs (degrade faster, used in flea collars, dips, fly, ant, roach baits)
  • parathion, malathion, chlorpyrifos
  • high water solubility and acute toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

OPs mechanism of action

A
  • irreversible inhibition of acetylcholine esterase activity
  • cholinergic overstimulation within minutes to hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clinical signs of anti-esterase toxicity

A
  • may affect muscarinic receptors, nicotinic receptors, and CNS
  • signs may last 1-5 days
  • in acute poisoning the primary clinical signs may be respiratory distress and collapse followed by death due to respiratory muscle paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

signs associated with muscarininc receptor overstimulation

A

SLUDGE-M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

signs associated with nicotinic receptors overstimulation

A

muscle fasiculations beginning with face, eyelids, and tongue, generalized tremors, weakness, paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

signs associated with CNS overstimulation

A

respiratory depression, ataxia, nervousness, clonic-tonic seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

specific clinical signs associated with OP toxicity

A
  • horses show clinical signs of colic and dehydration
  • rumen stasis in cattle, but no miosis
  • cattle and sheep commonly show severe depression
  • CNS stimulation in dogs and cats, progressing to convulsions
  • Chlorpyrifos causes more severe nicotinic signs in cats due to muscarinic tolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how to diagnose anticholinesterase toxicity

A
  • appropriate history and clinical signs
  • atropine challenge
  • decreased RBC AChE (inhibited > 50%)
  • non-specific pathology, may see pulmonary edema and petechial hemorrhage in GI mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

atropine challenge

A
  • administer pre-anesthetic dose
  • wait 15 mins to observe for normal signs of atropine (dry mouth, mydriasis, increases heart rate)
  • if observed, toxicity NOT due to cholinesterase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

treating anti-esterase toxicity

A
  • GI decontamination, bathing for dermal exposure
  • atropine sulfate for muscarinic signs, dose to effect
    • will not stop nicotinic signs
  • oximes (2-PAM) can reactivate AChE
  • diazepam or barbituates for seizures
  • time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

OPIDN: Organophosphate-induced delayed neurotoxicity

A
  • OP compounds that produce significant inhibition of neuropathy target esterase (NTE) may cause delayed neuropathy
  • characterized by axonal degeneration of long motor neurons
  • hindlimb weakness, paralysis
  • NO treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ivermectin

A
  • produced by soil fungus Streptomyces avermitilis
  • worm medication in dogs/cats
  • antihelminthic in livestock
  • dogs: 6-24 ug/kg is heartworm preventive dose but 200 ug/kg can cause ataxia, disorientation
  • collies, shepherds, shelties- 80/100 ug/kg causes toxicity because BBB does not block ivermectin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of ivermectin

A
  • drugs act as a GABAA receptor agonist
  • increase GABA release, enhances GABA binding and is a direct GABA receptor agonist
  • Increased inhibitory input decreases ability to respond to other stimuli
  • can see cumulative toxicity with repeat doses due to long half life (2-3 days)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clinical signs of Ivermectin toxicity

A
  • Onset time is hours to 1 day
  • affects CNS: ataxia, disorientation, lethargy, mydriasis, coma, blindness, some bradycardia
  • Recumbency and seizures more common in collies
  • Respiratory distress typically precedes death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diagnosis of Ivermectin toxicity

A
  • history of administration
  • brain ivermectin concentrations >100ppb
  • can also measure in GI content, liver, fat, feces
  • no visible lesions, no diagnostic bloodwork
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

treatment of ivermectin toxicity

A
  • GI contamination for recent exposures (multi doses of activated charcoal)
  • Supportive care including fluid and electrolyte therapy
    • epinephrine
    • short acting barbiturate for convulsions (no benzos)
  • Testing before administering higher doses of ivermectin is prudent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Prognosis of ivermectin toxicity

A

Good for non-susceptible breeds of dogs if exposed to <5 mg/kg but guarded at dosages > 5 mg/kg for any breed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

other rodenticides that affect the CNS

A
  • Bromethalin
  • Nicotine (Blackleaf 40)
  • Metaldehyde
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bromethalin

A
  • Single dose rodenticide
  • kills in 3-5 days so may see delayed toxicosis (trick the rats)
  • parent and metabolite uncouple oxidative phosphorylation in CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nicotine

A
  • Usually stimulate then block nicotinic ACh receptor
  • LD50 1-2 mg/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

metaldehyde

A
  • sources include fuel for small heaters and molluscicides
  • 3-4 oz bait toxic to average size dog, sheep
  • metabolized to acetaldehyde = CNS excitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

mycotoxins

A
  • Fungal metabolites which cause pathological, physiological and/or biochemical alterations usually on several organ systems
  • Can affect all species
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

slaframine

A
  • Produced by “Black patch” fungus on red clover
    • rain, high humidity, cool weather triggers growth
  • Occurs regularly in central, south-eastern and southwestern states of the USA
    • = an ACh mimic, primarily acts as a muscarinic cholinergic agonist, especially in exocrine glands
  • Most commonly in horses and cattle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

clinical signs of Slaframine

A
  • Copious salivation (“slobbers”) primary sign
    • may be the only clinical sign
  • Bloat, diarrhea, frequent urination
  • May see feed refusal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diagnosis of Slaframine toxicity

A
  • Diagnosed by consumption of clover, identification of black path in clover
  • Differentiate from OPs, botulism
28
Q

Treatment of Slaframine toxicity

A
  • Remove source, maintain hydration and electrolytes
  • Can treat with atropine
  • Clinical signs cease within 48 hours of the animals being removed from contaminated pasture (removal and cessation of salivation indicates direct diagnosis)
  • Rarely fatal
29
Q

Fumonisin

A
  • Metabolite of Fusarium spp. (important toxin is fumonisin B1)
  • Found almost exclusively on corn
  • Usually occurs in years of drought followed by wet weather
  • Presence of Fusarium spp. is not indicative of fumonisin
30
Q

MOA of Fusarium

A
  • Acts by inhibition of sphingosine-N-Acetyltransferase causing increased levels of spinganine, which is cytotoxic
  • Also affects vascular endothelial cells leading to stroke, hepatic injury, and pulmonary edema
31
Q

Susceptible species to fumonisin

A

Susceptible species include horses, ponies, swine, and rabbits

32
Q

2 diseases linked to fumonsins

A
  • Equine leucoencephalomalacia (ELEM)
  • Porcine pulmonary edema (PPE)
33
Q

Porcine pulmonary edema

A
  • CS: inactivity, increased RR, and decreased HR
  • signs occur about 12 hours before development of pulmonary edema
  • Develop lethal pulmonary edema within 4-7 days of consuming contaminated feed
  • Respiratory distress, manifested as increased RR and effort with abdominal and open mouth breathing, occurs within hours of death (cyanosis of MM)
34
Q

diagnosis of PPE

A
  • Analysis of feed for fumonisin in conjunction with clinical signs
  • An increase in serum and tissue sphingoid bases is one of the earliest and most specific biochemical change
  • Increase liver enzymes, total bilirubin, bile acids, and cholesterol
  • Post-mortem pulmonary pathology, indicating pulmonary edema, hepatic lesions, necrosis
35
Q

Equine Leukoencephalomalacia

A
  • Most common in late/early winter
  • Main target is brain and liver
    • ​acute onset of CNS signs that get progressively worse over hours
    • Hyperexcitability, mania, profuse sweating are terminal signs
  • Hepatotoxicity
    • jaundice, hepatic encephalopathy
    • coma and convulsions from hepatic encephalopathy are terminal)
  • Nearly 100% mortality rate
36
Q

Diagnosis of ELEM

A
  • Analysis of feed for fumonisin in conjunction with CSs
  • Severe liver injury and lesions
    • elevated liver injury and lesions
    • increased liver enzymes such as ALP, ALT, sorbitol dehydrogenase, GGT, and total bilirubin and bile acids
  • Post-mortem CNS necrosis and liquefaction
37
Q

treatment of fumonisin toxicity

A
  • No treatment available
  • Isolate affected animals to prevent injury to themselves and others
  • Change feed
  • Pigs usually recover within 48 hours of removing contaminated feed
38
Q

tremorgenic mycotoxins

A
  • Fungi of genera Penicillium, Aspergillus, Claviceps
    • elicit intermittent/sustained tremors in vertebrates
    • sources include food, stored grains/nuts, forage for livestock, garbage, compost
39
Q

MOA of tremorgenic mycotoxins

A

release of neurotransmitters from synaptosomes in the CNS

40
Q

Clinical signs of tremorgenic mycotoxins

A

diminished activity and immobility followed by hyperexcitability, muscle tremor, ataxia, tetanic seizures, convulsions

41
Q

ammoniated feed toxicosis

A
  • Non-protein nitrogen sources (urea, ammonium salts) are added to cattle feed
  • Found in high concentrations in mineral licks
  • Leads to excitablility “bovine bonkers”
42
Q

species affected by ammoniated feed toxicosis

A
  • bovine, caprine, ovine
    • ruminants are much more susceptible
    • calves can be affected though milk
43
Q

clinical signs of ammonia toxicosis/imidazoles

A
  • Hyperexcitability
    • ​nervousness, rapid blinking, dilated pupils, trembling, ataxia, rapid respiration, SLUD, tonic convulsions induced by stimuli
  • Animals will alternate between hyperexcitability and “normal” behavior if caused by imidazoles
  • rapid onset
    • 15 mins to several hours (death within 24 hours)
    • for ammonia toxicity, death occurs when blood ammonia >2 mg/dl
44
Q

diagnosis of ammonia toxicosis

A
  • Hx of exposure
  • Clinical signs very important
  • Differentials: OP pesticides, cyanide, grain overload, meningitis, encephalitis
  • Analysis of feed or blood/rumen fluid for ammonia levels
  • Increased ammonia, glucose, BUN, and decreased blood pH may help diagnose NPN ovedose
45
Q

Treatment of Ammonia Toxicosis - imidazole

A
  • No treatment, just feed removal
  • sedation may help prevent self-mutilation
  • milking out cows that have affected calves
  • prognosis is good in adults if feed is removed quickly
46
Q

treatment of NPN overdose toxicosis

A
  • No specific treatment
  • can try giving 5-10 gallons of cold water and 1 gallon vinegar by stomach tube
    • cold reduces urease activity and vinegar acidifies the rumen to convert ammonia to less absorbable form
  • prognosis is poor for recumbent animals
47
Q

strychnine

A
  • from seeds of Strychnos-nux vomica
  • Alkaloid used to control pocket gophers
  • Restricted-use pesticide
  • Often used as a malicious poison
  • LD50 ranges from 0.5-3 mg/kg, birds are higher
48
Q

strychnine MOA

A
  • Rapidly absorbed and distributed in blood, liver, kidney
  • Rapidly eliminated - complete in 48-72 hours
  • Competitive antagonist at postsynaptic spinal cord and medulla glycine receptors
  • Glycine is an inhibitory transmitter, so antagonism results in disinhibition (stimulation) of all muscles
49
Q

clinical signs of strychnine toxicity

A
  • Rapid onset (10-120mins) with little to no vomiting
  • Begins with anxiety, restlessness, stiff neck and gait, “grinning” as facial muscles stiffen, ears twitch
  • Proceeds to violent tetanic seizures initiated by external stimuli, frequency increases with time, respiratory distress
  • Sawhorse stance, rigid extension of all 4 limbs
  • Death from respiratory failure (asphyxiation during seizure), exhaustion
50
Q

diagnosis of Strychnine toxicity

A
  • clinical signs - tetanic seizures and sawhorse stance
  • hyperthermia in dogs
  • chemical analysis of bait, stomach contents, liver
  • Elevated CPK and LDH in serum
  • Lactic acidosis, hyperkalemia and leukocytosis common lab findings
  • Rule out other compounds that can cause seizures
51
Q

treatment of Strychnine toxicity

A
  • Primary goal is to control seizures and prevent asphyxiation
  • Administer phenobarb or methocarbamol
  • Emesis before any signs, gastric lavage once anesthetized - follow with activated charcoal and forced diuresis. MUST BE AGGRESSIVE
  • Ion trapping with ammonium chloride can be used to trap strychnine if animal is not acidotic
  • If acidosis develops, treat with bicarbonate
52
Q

salt toxicity

A
  • water deprivation (most common) or consumption of large amounts of salt
  • Most common in pigs but can be seen in cattle (or any animal)
53
Q

salt toxicity MOA

A
  • Mechanism is diffusion of sodium into CSF when plasma Na levels are high
  • When plasma Na levels drop, sodium leaves CSF slowly, attracting water to maintain osmotic balance
    • ​this increases CSF volume and pressure
54
Q

clinical signs of salt toxicity

A
  • Primarily CNS and include salivation, increased thirst, abdominal pain and diarrhea
  • Progressing over several days into: circling, wobbling, aimless wandering, head pressing, blindness, seizures and partial paralysis
  • Cattle may be beligerent and uncoordinated
  • Toxicity is about 2.2 g/kg in swine, equine, and bovine
55
Q

diagnosis of salt toxicity

A
  • Na levels > 160 meq/L, especially if CSF>serum
  • Brain Na >2000 ppm is diagnostic in swine and cattle
  • Differentiate from polio, lead, pesticides, encephalitis
56
Q

treatment of salt toxicosis

A
  • Slow rehydration (over a 2-3 day period)
  • Serum sodium levels should be lowered at a rate of 0.5-1mEq/L/hour
  • IV hyperosmotic fluids low in Na
  • Loop diuretic (furosemide) can be administered to prevent pulmonary edema during fluid therapy
57
Q

pharmaceuticals

A
  • Neuroactive substances - sleeping aids and anti-depressants
  • careless storage is the primary cause
  • top prescribed include Vicodin,Synthyroid, Zocor and Lipitor, Lisinopril
  • clinical signs can be similar to human toxicity
58
Q

alprazolam (Xanax)

A
  • Benzodiazepine
  • One of the top 10 human medications that the ASPCA receives calls for
59
Q

MOA of alprazolam

A

Acts at the limbic, thalamic, and hypothalamic level of CNS

60
Q

clinical signs of alprazolam toxicity

A
  • ataxia, depression, vomiting, tremors, tachycardia, diarrhea, and ptyalism
  • dangerously low body temp can also be present
  • signs usually appear within 30 mins of ingestion
  • some animals may show CNS excitation
61
Q

diagnosis of alprazolam toxicity

A

Based on suspected ingestion and clinical signs

62
Q

treatment of alprazolam toxicity

A
  • include standard decontamination procedures:
    • induce emesis with apomorphine if the ingestion is recent and no signs are present
    • Use gastric lavage with activated charcoal if toxic dose
  • flumazenil may be used for severe CNS depression associated with toxicosis
  • close monitoring is needed
  • additional treatment includes fluids and medications to support respiratory function
63
Q

zolpidem (Ambien)

A
  • Sleep aid that acts in a similar way as the benzodiazepines
    • non-benzo hypnotic drug
  • Another top 10 human medication that the ASPCA receives calls for
64
Q

MOA for Zolpidem

A
  • inhibits neuronal excitation by binding to the benzo omega-1 receptor
  • rapid absorption from GI tract and highly bioavailable
    • clinical signs typically resolve by 12 hours in dogs
65
Q

clinical signs of Zolpidem toxicity

A

Ataxia, vomiting, lethargy, disorientation, hypersalivation, hyperactivity and panting also possible

66
Q

diagnosis of Zolpidem toxicity

A

Based on suspected ingestion and clinical signs

67
Q

treatment of Zolpidem toxicity

A
  • Treatment is supportive and symptomatic
    • for mild signs, keep the pet quiet and in a safe place may be enough
    • if excitement develops, symptomatic treatment should be given and will vary with the signs and their intensity

Toxicology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions