Brainscape's Knowledge GenomeTM

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


See full index

Toxicology Final > Neurotoxicants > Flashcards

Neurotoxicants Flashcards

1
Q

What is the mechanism of organophosphates?

A

It is an acetylcholinesterase inhibitor, thus it inhibits the breakdown of acetylcholine at the synapse. When ACh builds up in the synapse, over stimulation of ACh receptors occurs at both muscarinic and nicotinic receptors.

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

What are the signs of organophosphate toxicity at the nicotinic receptor?

A

Muscle twitching

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

What are signs of organophosphate toxcitity at the muscarinic receptor?

A

SLUDGE parasympathetic signs (Salivation, Lacrimation, Urination, Defecation, GI, Exocrine glands)

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

What are general CNS signs associated with organophosphate toxicity?

A

Respiratory depression, ataxia, nervousness, clonic-tonic seizures

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

What are species specific signs of organophosphate toxicity in Cats, Dogs, Horses, Cattle, and Sheep?

A

Cats: CNS stimulation progressing to convulsions. Will show more nicotinic responses than dogs.
Dogs: CNS stimulation progressing to convulsions
Horses: Colic and dehydration
Cattle: Rumen stasis without miosis and severe depression
Sheep: Severe depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do you diagnose organophosphate toxicity?

A

Atropine Challenge: Administering an acetylcholine antagonist should greatly increase sympathetic effects. If you do not see sympathetic effects (mydriasis, dry mouth, increased HR), then it is likely organophosphates.
Can also Dx by clinical signs and seeing decreased RBC AChE.

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

How do you treat organophosphate toxicity if it has been under 24 hours?

A

Use of Praladoximine (2-PAM) to stop the “aging” process of organophosphates.
Atropine to stop muscarinic effects
Diazepam or barbituates to stop seizures
GI decontamination/bathing to remove from skin

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

What is the process behind delayed organophosphate neurotoxicity?

A

Chronic exposure causes a slow buildup of organophosphates that causes a delayed neuropathy characterized by axonal degeneration of long motor neurons. Animals will present with intact senses, but with hindlimb weakness/paralysis.

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

Pathologically, what happens to the body in organophosphate toxicity?

A

Vacuolization of brain tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the mechanism of Ivermectin toxcicity?

A

Ivermectin increases GABA release, enhances GABA binding and is a direct GABA receptor agonist causing inhibitory effects on the body and inability to respond to stimuli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical signs of Ivermectin toxcicity?

A

Ataxia, disorientation, lethargy, mydriasis, coma, blindness, some bradycardia.
Recumbancy and seizures (especially in Collies)
Respiratory distress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where can ivermectin levels be measured?

A

Brain, GI contents, liver, fat, and feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you treat recently ingested ivermectin?

A

GI decontamination with activated charcoal - multiple doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What anticonvulsant would you NOT use in Ivermectin toxcicity?

A

Benzodiazepines (It’s GABA modulating effects makes the CNS inhibitory effects worse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 3 CNS affecting Rodenticides?

A

Bromothalin (mitochondrial inhibitor)
Nicotine (block of Nicotinic receptors)
Metaldehyde (metabolite acetaldehyde causes CNS over excitation. Substance that causes hangovers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of Salaframine and where is it found?

A

Red clover mycotoxin.

It is an ACh mimic, and primarily acts as a muscarinic cholinergic agonist especially in exocrine glands = SLUDGE signs

17
Q

What are the clinical signs of Salaframine?

A

Excessive drooling “the slobbers”

Can also cause bloat, diarrhea, and frequent urination

18
Q

How do you treat Salaframine toxcicity?

A

Clinical signs abate within 48 hours of removing the clover from feed. SLUDGE signs can be treated with atropine. Maintain supportive care with fluids and electrolytes.

19
Q

What is the mechanism of Fumonisin and where is it found?

A

Metabolite of Fusarium spp. mold found on corn.
Causes inhibition of sphingosine-N-acetyltransferase causing increased levels of sphinganine, which is cytotoxic. Can affect vascular endothelial cells.

20
Q

What are clinical signs of Fumonisin in swine?

A

Cytotoxic effects on vascular endothelium causes porcine pulmonary edema and hepatic necrosis

21
Q

What are clinical signs of fumonisin in horses?

A

Cytotoxic effects targets brain and liver causing Equine Leukoencephalomalacia (equine frenzy) characterized by acute onset of anorexia, ataxia, circling, drowsiness, blindness, and hysteria that gets progressively worse.

22
Q

What is the treatment for Fumonisin toxicity?

A

There is none other than removing the contaminated feed. Swine tend to recover in 48 hours, but horses have a poor prognosis.

23
Q

What is the mechanism of tremorgenic mycotoxins and where is it found?

A

These types of mycotoxins are found in various types of mold that grow in improperly stored or spoiled food.
It causes the release of neurotransmitters from synaptosomes in the CNS leading to hyper-excitability and convulsions followed by CNS depression and paralysis.

24
Q

What do high levels of ammoniated feed cause?

A

Bovine bonkers

25
Q

How do you diagnose ammonia toxicity?

A

Analysis of feed or blood/ rumen fluid for ammonia levels (Normal blood ammonia concentration is

26
Q

How do you treat ammonia toxicity?

A

Dilute rumen ammonia by using 5-10 gallons of cold water and 1 gallon vinegar. Milk out cows so that calves don’t get ammonia buildup. Remove NPN sources from feed.

27
Q

What is the mechanism of Strychnine toxicity?

A

It is a competitive antagonist of glycine (which is an inhibitory transmitter) receptors causing over stimulation of muscles.

28
Q

What are the clinical signs of Strychnine toxicity?

A

Muscle ridgidity and “sawhorse” stance followed by seizures and death from respiratory distress or exhaustion.

29
Q

How do you diagnose Strychnine toxicity?

A

Clinical signs, and chemical analysis of stomach contents.

Can also check for elevated CPK and LDH, or lactic acidosis, hyperkalemia and leukocytosis from muscle destruction.

30
Q

How do you treat Strychnine toxicity if recently ingested?

A

Must aggressively clear the substance from the system as it is rapidly absorbed: Emesis, gastric lavage, activated charcoal, fluids and forced diuresis.
Ammonium chloride can be used to trap strychnine if animal is not acidotic.

31
Q

How do you treat Strychnine toxicity once signs occur?

A

Primary goal is to control seizures and prevent asphyxiation: Use of anti-seizure medication (Diazepam, phenobarbitol, methocarbamol), use of ventilator if necessary.
Ammonium chloride can be used to trap strychnine if animal is not acidotic.
Bicarbonate to treat acidosis.

32
Q

What is the mechanism of Na+ toxicity and how does it most commonly occur?

A

Usually happens in cases of dehydration.
When sodium is concentrated in the blood, it diffuses into the CNS which causes pressure and edema from osmotic water flow.

33
Q

What are the clinical signs of sodium toxicity?

A

Salivation, increased thirst, abdominal pain and diarrhea followed by circling, ataxia, head pressing, blindness, seizures and partial paralysis.

34
Q

How do you treat sodium toxicity?

A

Slow rehydration with hyperosmotic fluids low in Na+ (Hyperosmotic so that fluid is drawn back into circulation rather than the sodium heavy CNS)
Furosemide to prevent pulmonary edema from fluid therapy and to flush out sodium.
Mannitol to protect kidneys

35
Q

How do you treat Alprazolam toxicity?

A

Flumazenil (GABAa antagonist), may be used for severe CNS depression associated with toxicosis, otherwise use fluid therapy and respiratory support

36
Q

What are the clinical signs of Alprazolam (Xanax) toxicity?

A

Alprazolam acts at the limbic, thalamic, and hypothalamic level of CNS causing ataxia, depression, vomiting, tremors, tachycardia, diarrhea and ptyalism (hypersalivation).

37
Q

What is the mechanism of Zolpidem (Ambien) toxicity?

A

Acts similar to benzodiazepines and binds several GABA subunits while enhances GABA signaling to inhibit neuronal excitation.

Toxicology Final (6 decks)

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