Brainscape's Knowledge GenomeTM

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


See full index

Veterinary Toxicology > CNS Stimulants > Flashcards

CNS Stimulants Flashcards

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

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

A

those in the hippocampus

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

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

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

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

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

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

A

horses and small ruminants

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

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

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

Tetanus, dog:

A
  • sawhorse stance
  • fixed stare
  • ears pinned back
  • sardonic grin from excessive contraction of facial muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is strychnine poisoning most common?

A

Pacific Northwest

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What 3 things characterize metaldehyde toxicosis?

A
  1. CNS signs
  2. metabolic acidosis
  3. respiratory alkalosis
26
Q

What causes the metabolic acidosis of metaldehyde poisoning? CNS signs?

A

metabolism of acetaldehyde into acetic acid

decreases brain concentrations of GABA, NE, and serotonin and increases monoamine oxidase activity (breaks down catecholamines)

27
Q

What are the most common CNS/neuromuscular and ANS effects of metaldehyde toxicosis? What causes death?

A
  • 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
Q

What is the best diagnosis of metaldehyde poisoning? How else can it be diagnosed?

A

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
Q

What are the 5 major symptomatic and supportive treatments of metaldehyde toxicosis?

A
  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
Q

What are 2 possible sources of fluoroacetate (compound 1080)? What is current use in the US restricted to?

A
  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
Q

What metabolic steps lead up to fluoroacetate toxicosis?

A
  • undergoes hydrolysis to monofluoroacetic acid (MFAA)
  • MFAA enters a series of reactions leading to inhibition of the TCA cycle
32
Q

What effect does fluoroacetate have on the TCA cycle?

A

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
Q

What are the 3 results of aconitase inhibition in fluoroacetate toxicosis?

A
  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
Q

What tissues are most susceptible to fluoroacetate toxicosis? Why?

A

brain and heart —> high energy requirement will not be met due to TCA cycle blockade

35
Q

What 2 systems are most affected by fluoroacetate poisoning? What clinical signs are common in dogs?

A

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
Q

What are the characteristic signs of fluoroacetate in cats, horses, ruminants, and swine?

A

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
Q

Why is treatment of fluoroacetate difficult?

A

rapid onset of toxicosis - animals often die before getting veterinary attention

38
Q

What 2 treatments can improve survival of fluoroacetate toxicosis?

A
  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
Q

Most organochlorines are banned in the US and Canada. What 2 have limited use? What was approved to treat malaria?

A
  1. lindane
  2. methoxyclor
    - persist in the environment, bioaccumulate in food chains, and are carcinogenic

DDT

40
Q

Which species are especially susceptible to organochlorine toxicosis? How is it excreted?

A

cats

bile and urine

41
Q

What is the mechanism of toxicity of DDT-type organochlorines? Cyclodienes?

A

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
Q

What 3 things does chronic exposure to DDT-type organochlorines lead to?

A
  1. endocrine disruption
  2. estrogenic effects
  3. eggshell thinning in birds
43
Q

What are the 6 early signs of organochlorine toxicosis?

A

NERVOUS SIGNS:

  1. agitation
  2. tremors
  3. hyperexcitability
  4. nervousness
  5. ataxia
  6. aggressiveness
44
Q

What are the advanced signs of organochlorine toxicosis?

A

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
Q

What are the 3 main symptomatic and supportive therapies used in organochlorine toxicosis?

A
  1. Barbiturates for light sedation
  2. Methocarbamol musle relaxant for convulsions
  3. maintain airway patency with supplemental oxygen
46
Q

What 3 species are most susceptible to sodium ion toxicosis?

A
  1. swine
  2. cattle
  3. poultry
47
Q

What are the 2 types of sodium ion toxicity?

A
  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
Q

In what 2 situations does hypernatremia occur? What are the 2 main causes?

A
  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
Q

What is the mechanism of toxicity of sodium ion toxicity?

A
  • GI mucosal irritation —> anorexia, vomiting, diarrhea, dehydration, electrolyte imbalance
  • sodium is rapidly absorbed from the GI tract and distributted throughout the body
50
Q

How does plasma sodium concentration affect movement to CSF?

A

when plasma concentrations increases above normal (> 135-155 mEq/L), sodium passively diffuses into CSF, but requires active transport to be removed

51
Q

How does sodium in the CSF cause CNS signs? What happens when re-hydration occurs too rapidly?

A
  • 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
Q

What is the basic tenet of fluid shifts?

A

water always follows sodium

53
Q

Sodium ion toxicity:

A
54
Q

What clinical signs are common in swine with sodium ion toxicity?

A
  • 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
Q

How does sodium ion toxicity cause bloat in cattle? What are some other clinical signs?

A

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
Q

What are the main clinical signs of sodium ion toxicity in poultry and dogs?

A

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
Q

How is sodium ion toxicity diagnosed?

A
  • history and clinical signs
  • measurement of serum and CSF/brain sodium levels
  • assessment of hydration/dehydration status by PCV, and urine specific gravity
58
Q

How should sodium ion toxicity be treated?

A

SLOW - correct free water deficit over 48-72 hours

59
Q

How is free water deficit calculated?

A
60
Q

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?

A

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
Q

What are 4 treatments used to relieve cerebral edema from sodium ion toxicity treatment?

A
  1. Mannitol
  2. Glycerin
  3. Dexamethasone
  4. Dimethyl sulfoxide

Veterinary Toxicology (29 decks)

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