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Veterinary Toxicology > CNS Stimulants & Depressants > Flashcards

CNS Stimulants & Depressants Flashcards

1
Q

What 3 methylxanthines commonly cause toxicosis?

A
  1. theobromine
  2. caffeine
  3. theophylline
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2
Q

What are the main sources of theobromine? In what species is toxicity most common? What causes most poisonings? Which ones are the most dangerous?

A

cocoa beans, chocolate, cocoa bean shells, mulch

dogs, especially during holidays (Easter, Halloween, Christmas)

  • milk chocolate
  • baking chocolate
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3
Q

When is theobromine toxicosis common in horses?

A

when cocoa bean hulls or waste are used as bedding

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4
Q

What are the main sources of caffeine? What causes the most poisoning?

A

coffee, tea, chocolate, soft drinks, human/veterinary medications

caffeine tablet ingestion in dogs

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5
Q

What are the main sources of theophylline?

A

tea and medications for asthma (aminophylline)

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6
Q

Why are dogs must susceptible to methylxanthine toxicosis? When is toxicosis seen in horses?

A

eating habits

illegal use of caffeine to hype race horses

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7
Q

What barriers is caffeine able to cross? How does metabolism occur?

A

BBB, placenta, mammary glands

occurs in the liver by microsomal enzymes, undergoing demethylation and phase II conjugation

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8
Q

What process does caffeine significantly undergo during metabolism?

A

enterohepatic recirculation - metabolites excreted in the bile are reconverted to methylxanthines in the intestine and reabsorbed

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9
Q

How does theobromine absorption compare to caffeine? Excretion?

A

absorbed much slower than caffein, reaching plasma peak levels in 10 hours

excreted slowly in dogs

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10
Q

What is the most relevant mechanism of toxicity of methylxanthines?

A

competitive antagonism of adenosine receptors, causing CNS and cardiac stimulation

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11
Q

What are 4 additional mechanisms of toxicity of methylxanthines?

A
  1. elevates intracellular calcium concentrations, which increases skeletal and cardiac muscle contractility and decreases calcium sequestration in SR and mitochondria by releasing it into cytosol
  2. inhibits phosphodiesterase to increase cAMP levels
  3. synthesizes and releases catecholamines (caffeine)
  4. antagonizes benzodiazepine receptors
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12
Q

What is the characteristic clinical sign of caffeine toxicosis in dogs? What are some other signs?

A

bouncing effect when standing dog is lifted a few inches off the floor and dropped

  • agitation, hyperactivity, tremors, seizures
  • abnormal behavior, panting, tachycardia
  • weakness
  • ataxia, clonic convulsions
  • vomiting, diarrhea, diuresis, dehydration
  • hypokalemia
  • hypertension, cyanosis
  • coma
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13
Q

What causes death in caffeine toxicosis?

A

cardiac arrhythmias or respiratory failure

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14
Q

What are the main clinical signs of theobromine toxicosis?

A
  • CNS excitation with restlessness, tremors, seizures, ataxia, and hyperthermia
  • panting, polyuria, polydipsia, vomiting, diarrhea, dehydration
  • cardiac arrhythmias
  • weakness, coma, death from cardiac or respiratory failure
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15
Q

What are the main clinical signs of theophylline toxicosis?

A
  • nausea, vomiting, abdominal pain
  • hypotension and cardiac arrhythmias
  • muscle tremors, weakness
  • agitation, seizures, hyperactivity, behavioral abnormalities
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16
Q

How is methylxanthine toxicosis disgnosed?

A
  • history of exposure and clinical signs
  • measurement of methylxanthines and their metabolite concentrations in stomach contents, plasma/serum, urine, or liver
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17
Q

There is no antidote for methylxanthine toxicosis. What are the 2 major ways to treat it?

A
  1. DECONTAMINATE: emesis with apomorphine or H2O2, gastric lavage, activated charcoal
  2. LIFE SUPPORT: relieve respiratory difficulties by maintaining airway patency and giving artificial respiration, IV fluids to maintain renal perfusion, increase excretion, and correct electrolyte imbalances
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18
Q

What are the main 3 symptoms of methylxanthine toxicosis treated?

A
  1. seizures/hyperactivity - Diazepam, Midazolam, Barbiturate
  2. tremors - Methocarbamol
  3. cardiac dysfunction - Atropine (bradycardia), Propranolol (tachyarrhythmias), Lidocaine (premature ventricular contractions)
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19
Q

Where is water hemlock (Cicuta) found? What species are most susceptible to toxicity? Why is it so significant?

A

swamps, marshes, streams, meadows, irrigation ditches

cattle and sheep

among the most violently toxic plants known

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20
Q

What are the 2 toxic principles of water hemlock (Cicuta)? Where are they most concentrated in the plant?

A
  1. cicutoxin
  2. cicutal

chambered rootstock and young shoots, but all parts are toxic

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21
Q

What is the mechanism of action of water hemlock (Cicuta)?

A

cicutoxin is a potent convulsant that antagonizes GABA

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22
Q

What course does water hemlock (Cicuta) toxicosis have? What are the most common clinical signs?

A

paracute violent course with intense muscular activity and sudden death

  • salivation, urination, defecation
  • muscular twitching and spasms
  • vigorous chewing movements, teeth griding (tongues chewed off)
  • ataxia, seizures that knock animal off its feet
  • running fits
  • coma and death from respiratory paralysis
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23
Q

What are the most common treatments of water hemlock (Cicuta) toxicosis?

A
  • induce emesis before onset of clinical signs
  • give laxatives to speed up removal of plants from GIT
  • perform rumenectomy to remove plant material
  • IV Pentobarbital (prevented death in sheep)
24
Q

What is commonly used to neutralize water hemlock (Cicuta) toxicosis? Why is treatment difficult?

A

acetic acid given orally in cattle

paracute nature of toxicosis

25
Q

Wha are the 4 toxic principles of bracken fern (Pteridium aquilinum)? What does it commonly contaminate?

A
  1. thiaminase**
  2. ptaquiloside
  3. cyanogenic glycoside
  4. bone marrow factor

hay

26
Q

What is the mechanism of toxicity of bracken fern (Pteridium aquilinum) in horses and cattle?

A

HORSE - thiaminase destroys vitamin B1 in GI tract before absorption, which results in impaired carbohydrate metabolism, decreased ATP production, and pyruvate accumulation

CATTLE - bone marrow syndrome

27
Q

Bracken fern toxicosis, thiaminase mechansism:

A

DECREASED THIAMINE =
- decreased ACh
- decrease myelin production
- decreased glutamate, GABA, and aspartate (inhibitory)
- decreased ATP

28
Q

What are the main clinical signs of Bracken fern toxicity in horses?

A
  • anorexia, emaciation
  • incoordination, wide-based or crouched stance
  • posterior paralysis
  • severe tremors, convulsions
  • opisthotonus, recumbency
  • lethargy, hyperthermia
  • weak and fast pulse, bradycardia
29
Q

How is Bracken fern toxicity treated?

A

thiamine administration

30
Q

What is the main sources of Ivermectin?

A

macrolide endectocides - anthelminitics for the treatment of roundworms, heartworm, lungworms, and strongylosis

31
Q

What species tend to develop ivermectin toxicity? What 3 are at the highest susceptibility?

A

dogs, cats, turtles, horses

  1. Collies/herding dogs
  2. turtles
  3. younger animals, like foals and kittens
32
Q

How does the absorption of ivermectin compare in ruminants and monogastric species? How is it excreted? How does the parent compound act?

A

less GI absorption (25%) in ruminants, more absorption (95%) in monogastrics

liver metabolism is low —> excreted in feces unchanged

persistent in the body —> concentrates in liver and fat, leading to cumulative toxicity

33
Q

Why are herding dogs very susceptible to ivermectin toxicity?

A

exclusion from the CNS depends on the P-glycoprotein efflux pump, and Collies, Shelties, English Sheepdogs, and Australian Shepherds tend to lack adequate levels of this protein

  • cellular bouncers!
34
Q

What is the mechanism of toxicity of ivermectin?

A

GABA agonist - stimulates presynaptic release of GABA and enhances its binding to postsynaptic receptors

GABA will open postsynaptic Cl- channels leading to the entry of negatively charged ions and hyperpolarization of neurons leading to flaccid paralysis in arthropods and nematodes

35
Q

What is the main clinical sign of ivermectin toxicity? What els can occur?

A

depression

  • disorientation, ataxia
  • decreased menace response
  • hyperesthesia, hyperthermia, apprehension
  • mydriasis
  • chewing fits, head pressing
  • emesis, anorexia, hypersalivation
  • cardiac arrhythmia, tremors, seizures
  • coma, death
36
Q

How do dogs with heartworm present with ivermectin toxicity?

A

shock-like syndrome: hypotension, pale mucous membranes, weak heart sounds, dyspnea, decreased skin temperature

37
Q

Response to what drug supports ivermectin toxicity diagnosis?

A

Physostigmine, which can reverse CNS depression

38
Q

There is no treatment for ivermectin toxicosis. What has been suggested to increase excretion?

A

IV lipid emulsion (Intralipid)

39
Q

Why is Physostigmine not necessarily recommended for symptomatic therapy of ivermectin toxicity? What is recommended for bradycardia?

A

can cause neuronal hypopolarization, but it is not a specific antagonist, so there may be an increase in adverse effects

Atropine

40
Q

What is the main source of Marijuana? What species are susceptible to toxicosis?

A

dried leaves, seeds, and stems of Cannabis sativa

  • dogs: consumption of owner supply
  • cattle consumption of fresh plants
41
Q

What is the main toxic principle of Marijuana?

A

THC (tetrahydrocannabinol)

42
Q

What is the most common cause of animal poisoning with Marijuana? What happens after absorption?

A

ingestion (small animals can be poisoned by inhalation)

undergoes significant first-pass effect when ingested (enterohepatic recirculation)

43
Q

What can increase the absorption of Marijuana? Why?

A

fatty foods

highly lipid soluble, allowing quick distribution into body fat, brain, liver, and kidney

44
Q

What is thought to be the mechanism of toxicity of Marijuana?

A

THC acts on cholinergic, dopaminergic, GABA, noradrenergic, and serotonergic receptors

45
Q

What receptors cannabinoid receptors have been identified in the CNS and PNS? What effect does this lead to?

A

CNS = CB1
PNS = CB2

potent antiemetic - inhibits the release of emetic NT via stimulation of CB1 receptors

46
Q

What is the biphasic behavior change associated with Marijuana toxicity? What other clinical signs are seen?

A

euphoria followed by depression

  • ataxia, tremors
  • muscle weakness
  • agitation, apprehension, disorientation
  • hypermetria, vocalization
  • mydriasis, “glazed” eyes, nystagmus
  • salivation, vomiting, diarrhea
  • hypotension, hypo/hyperthermia, brady/tachycardia
  • recumbency, coma
47
Q

What is the paradox of Marijuana toxicity? What are the 3 possible mechanisms?

A

potent antiemetic, but also causes emesis

  1. cannabinoids act as a partial agonist of CB1, but can become an antagonist
  2. other components of cannabis may be emetics
  3. genetic variation in metabolic enzymes in some individuals may result in excessive levels of metabolites of cannabinoids that promote vomiting
48
Q

How is cannabinoid presence tested?

A

detection in stomach contents and urine

  • can be detected in urine for several days due to its lipophilicity and enterohepatic recirculation (IV lipid emulsion can increase excretion)
49
Q

What are the 4 main symptomatic treatments of cannabinoid toxicosis?

A
  1. bradycardia - Atropine
  2. dehydration, urine output - IV fluids
  3. vomiting - antiemetics
  4. CNS stimulation - Benzodiazepines
50
Q

What is the toxic principle of white snakeroot (Eupatorium rugosum)? What species are most susceptible? Where in the US do most problems occur?

A

tremetone

goats*, cattle, horses, sheep, dog, cat

OH, IN, IL, NC, MO

51
Q

What is thought to be the toxic principle of white snakeroot? What is required to cause toxicosis?

A

acts like rotenone - blocks electron transport in the mitochondria to decrease ATP production and impair nerve conduction

cumulative toxin —> repeated low dose exposures

52
Q

How is white snakeroot toxicosis spread? Why is this so dangerous?

A

though milk —> lactating animals less susceptible

pasteurization does not detoxify milk

53
Q

What are the most prominent features of white snakeroot toxicosis? What other clinical signs occur?

A

muscle tremors and weakness —> trembles, milk fever

  • reluctance to move*
  • sluggish behavior*
  • ataxia
  • stiff gait
54
Q

What are the severe signs of white snakeroot toxicity? Clinical signs in horses?

A
  • severe CNS depression*
  • sternal recumbency
  • coma, death
  • acetone odor in breath and urine

sweating, cardiovascular signs (CHF)

55
Q

What other 2 plants are known to cause the same clinical signs of white snakeroot toxicity in horses?

A
  1. Isocoma wrightii (rayless goldenrod)
  2. burroweed
56
Q

What enhances the elimination of white snakeroot in cattle? What species require symptomatic treatment?

A

milking (discard milk)

horses

Veterinary Toxicology (29 decks)

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