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Veterinary Toxicology > CNS Stimulants > Flashcards

CNS Stimulants Flashcards

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1
Q

What 3 features of neurons adapted for rapid signal transmission predispose the CNS to xenobiotics?

A
  1. high dependence on aerobic glycolysis for function - brain receives 20-25% of cardiac output
  2. extended length of axons
  3. limited capacity to regenerate
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2
Q

What type of neuron in the brain is able regenerate following injury?

A

those in the hippocampus

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3
Q

How does the CNS compensate for its vulnerability? What biochemical components enhance the effectiveness of these defense mechanisms?

A
  • BBB: capillary endothelium + astrocytic end feet
  • blood CSF barrier: capillary endothelium + CSF + ependymal cells

P-glycoproteins act as efflux pumps and enzymes metabolize possible toxicants/toxins

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4
Q

What are the direct and indirect effects of toxicants/toxins on the CNS?

A

DIRECT = impairment of of neurotransmission (functional), neuronopathies/myelinopathies/axonopathies (structural)

INDIRECT = impaired metabolism, ion homeostasis, and blood supply

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5
Q

What are the 3 classes of small molecule neurotransmitters commonly affected by toxicants/toxins?

A

CLASS I - acetylcholine

CLASS II (amines) - norepinephrine, epinephrine, dopamine, serotonin, histamine

CLASS III (amino acids) - GABA, glycine, glutamate, aspartate

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6
Q

What CNS neuropeptide and purine-based neurotransmitters are commonly affected by toxicants/toxins?

A

NEUROPEPTIDE - opioid peptides, tachykinins

PURINE-BASED - adenosine, ATP, AMP, ADP

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7
Q

What are the 3 actions that CNS toxicants undertake?

A
  1. cause CNS stimulation and/or seizures
  2. cause CNS depression
  3. cause mixed CNS signs
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8
Q

What are 2 sources of tetanus neurotoxin (TeNT)?

A
  1. tetanospasmin produced Clostridium tetani under anaerobic condition
  2. Clostridium tetani spores commonly present in the feces of horses
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9
Q

How do most animals come into contact with tetanus neurotoxin (TeNT)? What risk factors can increase chances of exposure?

A

deep puncture wounds

  • field surgery
  • castration
  • docking
  • retained placenta
  • shearing
  • umbilical infections
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10
Q

What species is most susceptible to tetanus neurotoxin (TeNT) toxicosis?

A

horses and small ruminants

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11
Q

What is the mechanism of toxicity of tetanus neurotoxin (TeNT)? What additional minor effect does it have?

A

zinc metalloprotease that gains access to CNS by retrograde transport along nerves and blood, which allows the light chain to cleave VAMP and block the release of glycine in the CNS resulting in a loss of inhibitor input

inhibits the release of GABA and ACh at NMJs

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12
Q

What are the 3 characteristic clinical signs of tetanus? What are some additional signs? What leads to death?

A
  1. severe rigidity of musculature resulting in a sawhorse stance
  2. locked jaw
  3. sardonic grin

hyperesthesia, convulsions, elevated tail, flared nostrils, sweating, cardiac arrhythmias, vasoconstriction, diminished urination and defecation, colic (sympathetic)

rigidity of muscles of respiration —> asphyxiation

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13
Q

Tetanus, dog:

A
  • sawhorse stance
  • fixed stare
  • ears pinned back
  • sardonic grin from excessive contraction of facial muscles
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14
Q

How is tetanus diagnosed? How is it treated? What drugs are used to control convulsions?

A

identification of Clostridium tetani in a culture of the wound

  • wound debridement
  • antibiotic therapy (penicillin)
  • antitoxin administration
  • keep animal in quiet, dark area to minimize convlusions
  • tranquilizers
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15
Q

What is strychnine? What is the main source? What species are most susceptible to toxicosis?

A

alkaloid derived from seeds/bark of Indian tree (Strychnos nux vomica and ignatti)

pesticides to control gophers*, moles, rats, prairie dogs, and squirrels

dogs

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16
Q

What is the mechanism of toxicity of strychnine?

A

competitively and reversibly antagonizes the inhibitory NT glycine in the spinal cord and medulla leading to uncontrolled reflex stimulation with extensor rigidity

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17
Q

Where is strychnine poisoning most common?

A

Pacific Northwest

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18
Q

What are the early signs of strychnine poisoning? What develops next?

A

apprehension, nervousness, tenseness, stiffness, excessive salivation

  • severe tetanic seizures with sawhorse stance initiated by touch, sound, or bright light
  • apnea
  • cyanosis
  • hyperthermia
  • mydriasis
  • strained facial expression
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19
Q

What does not occur during strychnine poisoning? What causes death?

A

loss of consciousness

medullary paralysis and exhaustion with rapid onset of rigor mortis

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20
Q

How is strychnine poisoning diagnosed?

A
  • history of exposure and clinical signs
  • presence of red or green dyed grain in vomitus, lavage washings, or stomach contents
  • chemical analysis of stomach contents and tissues
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21
Q

How is decontamination, symptomatic treatment, and supportive treatment carried out in strychnine poisoning?

A

emesis or gastric lavage followed by activated charcoal/cathartic administration

Barbiturates or Diazepam for convulsions and Methoarbamol for muscle relaxation

IV fluids to correct hypovolemia, respiratory assistance, hyperthermia correction

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22
Q

What is the main source of metaldehyde? What do its different formulations commonly contain?

A

molluscicide in slug and snail baits

arsenic, OPs, CMs

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23
Q

What species are most susceptible to metaldehyde poisoning? Where do most cases occur?

A

dogs and cats (looks like kibble and bait is flavored with molasses to attract snails/slugs)

coastal US

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24
Q

In what 2 ways is metaldehyde absorbed? What is suspected to do most of its metabolism?

A
  1. intact
  2. hydrolyzed by acidic stomach pH to acetaldehyde, which is subsequently oxidized into acetic acid

CYP450

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25
What 3 things characterize metaldehyde toxicosis?
1. CNS signs 2. metabolic acidosis 3. respiratory alkalosis
26
What causes the metabolic acidosis of metaldehyde poisoning? CNS signs?
metabolism of acetaldehyde into acetic acid decreases brain concentrations of GABA, NE, and serotonin and increases monoamine oxidase activity (breaks down catecholamines)
27
What are the most common CNS/neuromuscular and ANS effects of metaldehyde toxicosis? What causes death?
- tremors*, convulsions/seizures*, loss of blink reflex, blindness, nystagmus, hyperesthesia, ataxia, muscle spasms, opisthotonus - hyperthermia*, salivation, foaming at the mouth, panting, frothy diarrhea, cyanosis, hypotension, tachycardia, colic, sweating in horses * = shake and bake respiratory failure
28
What is the best diagnosis of metaldehyde poisoning? How else can it be diagnosed?
demonstration of metaldehyde in stomach contents - metaldehyde in vomitus, bait, serum, urine, and liver - history of exposure with clinical signs - acetaldehyde odor in stomach contents
29
What are the 5 major symptomatic and supportive treatments of metaldehyde toxicosis?
1. Diazepam and Acetylpromazine for seizures 2. Methocarbamol for muscle tremors 3. Barbiturate for severe tremores/seizures 4. crystalloid IV fluids for hemodynamic support and hydration 5. cold IV fluid and external cooling for hyperthermia (evaporative and direct)
30
What are 2 possible sources of fluoroacetate (compound 1080)? What is current use in the US restricted to?
1. plants (Dichapentalum, Acacia) in Australia, Brazil, and South Africa 2. pesticide use for the control of rodents, coyotes, wolves, and ground squirrels livestock protection collars for sheep and goats in MT, NM, SD, TX, and WY
31
What metabolic steps lead up to fluoroacetate toxicosis?
- undergoes hydrolysis to monofluoroacetic acid (MFAA) - MFAA enters a series of reactions leading to inhibition of the TCA cycle
32
What effect does fluoroacetate have on the TCA cycle?
hydrolysis of fluoroacetate into MFAA reacts with acetyl-CoA, forming fluroracetyl-CoA which combines with oxaloacetate to form the toxic fluorocitrate - fluorocitrate blocks aconitase, which takes part in the TCA
33
What are the 3 results of aconitase inhibition in fluoroacetate toxicosis?
1. interference with cellular respiration and metabolism of fats, CHOs, and proteins by the blockade of the TCA cycle 2. accumulation of citrate and lactase leading to acidosis 3. accumulated citrate and fluoride binds plasma calcium, leading to hypocalcemia and seizures
34
What tissues are most susceptible to fluoroacetate toxicosis? Why?
brain and heart ---> high energy requirement will not be met due to TCA cycle blockade
35
What 2 systems are most affected by fluoroacetate poisoning? What clinical signs are common in dogs?
CNS (excitation) and GI (hyperactivity) - anxiety, frenzied behavior (running fits*, howling) - seizures, hyperesthesia - tonic and clonic convulsions - hyperthermia - anoxia ---> respiratory failure - salivation, vomiting, urination, tenesmus, defecation - weakness, coma, death
36
What are the characteristic signs of fluoroacetate in cats, horses, ruminants, and swine?
CNS and cardiac signs - excitation, depression, vocalization, hyperesthesia, cardiac arrhythmias hyperesthesia, cardiac signs lethargy, salivation, tachycardia, tacypnea, dyspnea, staggering, trembling, collapse, teeth grinding, seizures, coma, death cardiac and nervous signs, vomiting
37
Why is treatment of fluoroacetate difficult?
rapid onset of toxicosis - animals often die before getting veterinary attention
38
What 2 treatments can improve survival of fluoroacetate toxicosis?
1. IV saline and sodium bicarbonate 2. acetamide in 5% dextrose (rather than glycerol monoacetate, which is difficult to get and is very painful after IM administration)
39
Most organochlorines are banned in the US and Canada. What 2 have limited use? What was approved to treat malaria?
1. lindane 2. methoxyclor - persist in the environment, bioaccumulate in food chains, and are carcinogenic DDT
40
Which species are especially susceptible to organochlorine toxicosis? How is it excreted?
cats bile and urine
41
What is the mechanism of toxicity of DDT-type organochlorines? Cyclodienes?
slows down the closing of Na+ channel and inhibits K+ efflux in CNS and peripheral nerves, diminishing the threshold for stimulation of nerves and increases neuron firing GABA antagonists - competitively inhibits binding of GABA to its receptor
42
What 3 things does chronic exposure to DDT-type organochlorines lead to?
1. endocrine disruption 2. estrogenic effects 3. eggshell thinning in birds
43
What are the 6 early signs of organochlorine toxicosis?
NERVOUS SIGNS: 1. agitation 2. tremors 3. hyperexcitability 4. nervousness 5. ataxia 6. aggressiveness
44
What are the advanced signs of organochlorine toxicosis?
MUSCULAR SIGNS - clonic-tonic seizures - opisthotonus - paddling - jaw clamping - hyperthermia - muscle fasciculations - abnormal posture - walking backward - paresthesia - excessive licking and chewing - coma and death
45
What are the 3 main symptomatic and supportive therapies used in organochlorine toxicosis?
1. Barbiturates for light sedation 2. Methocarbamol musle relaxant for convulsions 3. maintain airway patency with supplemental oxygen
46
What 3 species are most susceptible to sodium ion toxicosis?
1. swine 2. cattle 3. poultry
47
What are the 2 types of sodium ion toxicity?
1. DIRECT Na+ toxicity: excessive salt intake in water or feed, high salt milk substitutes, whey, inappropriate use of sodium-containing IV fluids ---> acute, signs in 24-48 hours 2. INDIRECT toxicity: water deprivation (swine and poultry!) ---> most common, chronic, signs in 4-7 days
48
In what 2 situations does hypernatremia occur? What are the 2 main causes?
1. Na+ content of ECF increases relative to free water content 2. free water in ECF is lost without compensatory decrease in sodium concentration - restricted water intake - third spacing: accumulation of water in transcellular space, like body cavities (pleural, peritoneal), joints, and GI tract
49
What is the mechanism of toxicity of sodium ion toxicity?
- GI mucosal irritation ---> anorexia, vomiting, diarrhea, dehydration, electrolyte imbalance - sodium is rapidly absorbed from the GI tract and distributted throughout the body
50
How does plasma sodium concentration affect movement to CSF?
when plasma concentrations increases above normal (> 135-155 mEq/L), sodium passively diffuses into CSF, but requires active transport to be removed
51
How does sodium in the CSF cause CNS signs? What happens when re-hydration occurs too rapidly?
- high [Na+] in CSF depresses glycolysis, which decreases the energy available for active transport needed to remove sodium from CSF - trapped Na+ causes dehydration. ofthe brain and rupture of blood vessels plasma Na+ returns to normal, but the Na+ trapped in the CSF attracts water due to osmotic gradient, causing cerebral edema
52
What is the basic tenet of fluid shifts?
water always follows sodium
53
Sodium ion toxicity:
54
What clinical signs are common in swine with sodium ion toxicity?
- restlessness, thirst - colic, vomiting, diarrhea, constipation - anorexia - pruritus - polyuria/anuria - aimless wandering, circling, head pressing, head jerking, pivoting - blindness, deafness - dog-sitting, lateral recumbency, paddling - clonic tonic seizures, opisthotonus - death
55
How does sodium ion toxicity cause bloat in cattle? What are some other clinical signs?
increased thirst causes aggressive sucking in air with water - incoordination - bellowing - fasciculation of facial muscles, ear twitching, sticking tongue out, seizures - fence walking, aimless wondering - blindness - partial paralysis - knuckling at the fetlocks - salivation, vomiting, diarrhea, abdominal pain, constipation, dehydration
56
What are the main clinical signs of sodium ion toxicity in poultry and dogs?
sudden death, thirst, dyspnea, fluid discharge from beak, ascites, wet droppings, weakness, paralysis of legs, depression rare and not life-threatening: GI signs (vomiting, diarrhea), polyuria, polydipsia, muscle tremors, seizures, depression
57
How is sodium ion toxicity diagnosed?
- history and clinical signs - measurement of serum and CSF/brain sodium levels - assessment of hydration/dehydration status by PCV, and urine specific gravity
58
How should sodium ion toxicity be treated?
SLOW - correct free water deficit over 48-72 hours
59
How is free water deficit calculated?
60
What fluids are recommended to reduce the incidence of iatrogenic cerebral edema from sodium ion toxicity treatment? What is commonly used to augment NaCl elimination?
hypertonic saline - Na+ levels of parenteral and oral fluids should closely match serum Na+ levels and gradually decrease as clinical signs subside Furosemide, a loop diuretic
61
What are 4 treatments used to relieve cerebral edema from sodium ion toxicity treatment?
1. Mannitol 2. Glycerin 3. Dexamethasone 4. Dimethyl sulfoxide

Veterinary Toxicology (29 decks)

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