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Toxicology > Lecture 8 - ANS Part II > Flashcards

Lecture 8 - ANS Part II Flashcards

1
Q

Nicotinic receptors are widespread, and in addition to the ___________ ganglia they are found in the ____ and _____.

A

autonomic, CNS, NMJ

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2
Q

Note that the ganglionic and NM nicotinic receptors can be distinguished using _____________ and ____________, that is, ganglionic nicotinic receptors are
sensitive to (blocked by) ____________ whereas NM nicotinic receptors are
sensitive to (blocked by) __________.

A

hexamethonium tubocurarine, hexamethonium, tubocurarine

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3
Q

What are the clinical signs of Nicotinic Stimulation?

A
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4
Q

Nicotinic receptors are located in both the _________ and _______
systems as well as in the _____.

A

sympathetic, parasympathetic, CNS

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5
Q

Where is Nicotine sourced from?

A

several plants, tobacco products,
nicotine gum (Nicorette), snuff, nicotine sulfate
(insecticides, immobilizing agent)

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6
Q

Nicotine is absorbed from?

A

GI and respiratory tracts, and
skin

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7
Q

Nicotine has potent _______ effect that limits absorption.

A

emetic

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8
Q

Where is Nicotine metbolized?

A

Metabolized in the liver, kidney and lungs

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9
Q

What is Nicotine’s mechanism of toxicity?

A

Release of Catecholamines esp. epinephrine

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10
Q

How do you treat Nicotine toxicosis?
1. Decontamination
– Emesis if orally exposed within past ______
– Gastric _________, activated _______, ________, ______ bowel irrigation
– For dermal exposure wash animal with ______ water and mild hand _________ detergent
2. Control seizures with a ________ (e.g., ?) or a ____________
3. Treat ___________: external cooling with tepid running water and/or fanning
4. Provide ________ pressure ventilation and supplemental _______
5. Provide symptomatic treatment, e.g., _______ crystalloid fluids for cardiovascular effects
6. Rarely, __________ may be indicated for severe bradycardia
7. Acidification of urine with _________ ________ to hasten nicotine excretion

A
  1. Decontamination
    – Emesis if orally exposed within past 1 h
    – Gastric lavage, activated charcoal, catharsis, whole
    bowl irrigation
    – For dermal exposure wash animal with warm water
    and mild hand dishwashing detergent
  2. Control seizures with a benzodiazepine (e.g.,
    diazepam, lorazepam) or a barbiturate
  3. Treat hyperthermia: external cooling with tepid
    running water and/or fanning
  4. Provide positive pressure ventilation and
    supplemental oxygen
  5. Provide symptomatic treatment, e.g., isotonic
    crystalloid fluids for cardiovascular effects
  6. Rarely, atropine may be indicated for severe
    bradycardia
  7. Acidification of urine with ammonium chloride
    to hasten nicotine excretion
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11
Q

What plant can be seen below?
Where can it be found? Be specific.

A

Tobacco (Nicotiana spp.)
* Annual/perennial, shrub (1-4ft), sticky
* Habitat: all US, SW states mainly
* Entire plant is toxic but
is largely unpalatable
– Risk of poisoning is low if good quality forage is available

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12
Q

What are the toxic principles of Tobacco?
What species are affected?

A
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13
Q

What are the general clinical signs of Tobacco (Nicotiana spp.) toxicosis?

A

Dullness, vomiting, salivation, abdominal cramps,
bloat, colic, diarrhea, frequent urination
* Muscular weakness, staggering, trembling,
shivering, spasms, muscle tremors, 3rd eyelid
protrusion, blindness, prostration, opisthotonus
* Irregular weak pulse, heart palpitation
* Elevated body temperature with cold extremities
* Diaphragmatic spasms, respiratory paralysis,
dyspnea and death

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14
Q

What is the primary clinical sign of Tobacco (Nicotiana spp.) toxicosis in swine?

A
  • In swine the primary problem is teratogenesis
    – Day 35 of gestation seems to be the end of the dangerous period
  • Pregnant sows may give birth to piglets
    with arthrogryposis
    – Prolongation of parturition ensues and kills
    many piglets from neonatal asphyxiation
  • Sows may not show signs of toxicosis
    before giving birth to malformed piglets
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15
Q

How do you diagnose Tobacco (Nicotiana spp.) toxicosis?

A
  • History of exposure and clinical signs
  • Confirm by identifying nicotine or other
    nicotine-like alkaloids in blood, urine, GI
    contents, liver or kidney
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16
Q

How do you treat Tobacco (Nicotianna spp.) toxicosis?

  • Decontamination
    – ________ or __________ lavage
    – Administer __________ _________
    * Most cases involve livestock, so decontamination is
    limited to administration of?
  • ___________ for parasympathetic effects
  • Artificial respiration and fluid therapy
A
  • Decontamination
    – Emesis or enterogastric lavage
    – Administer activated charcoal
    * Most cases involve livestock, so decontamination is
    limited to administration of activated charcoal
  • Atropine for parasympathetic effects
  • Artificial respiration and fluid therapy
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17
Q

What can be seen in the image below?

A

Conium maculatum
(Poison hemlock, conium, spotted hemlock)

Tea made from this plant killed Socrates in 400BC

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18
Q
  1. Describe Conium maculatum.
  2. What is its habitat?
  3. What are its toxic principles?
  4. What is the lethal dose of this plant? The early stages contain? The late stage?
A

See below

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19
Q

What species are effected by poison hemlock toxicosis? What is the MOT?

A
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20
Q

What are the clinical signs of poison hemolock toxicosis?

A
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21
Q

What plant is pictured below?
Where does it reside?

A

Lupinus (Lupine or Bluebonnet)
* Low bushy herbaceous perennial (12-26 in)
* Over 100 species in North America. Not all are toxic
* Occur throughout the US but mainly in Rocky Mountains westward

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22
Q

What are the toxic principles of Lupinus?
Where are the toxins most concentrated?

A

– > a dozen quinolizidine and piperidine alkaloids,
and anagyrine
– Toxins are most concentrated in pods & seeds

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23
Q

Lupinus MOT
MOT: the alkaloids are mainly ________ whereas anagyrine is ________
* Species: (4). Rare in ______ and ______ because they do not usually eat pods

A

MOT: the alkaloids are mainly nicotinic whereas
anagyrine is teratogenic
* Species: sheep, goats, swine, deer. Rare in cattle and horses because they do not usually eat pods

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24
Q

Which plant causes more deaths than any other plant in Montana, Idaho and Utah?

A

Lupinus

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25
Q

What are the clinical signs of Lupinus toxicosis in sheep?

A

Sheep: Labored breathing, depression,
salivation, ataxia, clonic spasms, seizures,
butting other animals and pressing against
the fence, respiratory failure, coma and death

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26
Q

What are the clinical signs of Lupinus toxicosis in cattle?

A

Excessive salivation, teeth- grinding, muscular weakness, ataxia,
recumbency, respiratory paralysis and death

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27
Q

What is this calf suffering from?
What may be present?
Where is this disease reported?

A

See below

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28
Q

How do you diagnose Poison Hemock and Lupinus toxicosis?

A
  • History of plant ingestion
  • Clinical signs
  • Chemical analysis of blood, stomach
    contents, liver or kidney
29
Q

How do you treat Poison Hemock and Lupinus toxicosis?

A
  • Nonspecific: activated charcoal, gastric
    lavage and assisted respiration
  • Avoid overexcitement and stress to animal
30
Q

What type of plant is pictured below? What toxin(s) does it contain?

A
  • Lobelia cardinalis (Cardinal
    flower)
    – Contains nicotinic alkaloids –
    lobeline, lobelidine and others
31
Q

What type of plant is pictured below? What toxin(s) does it contain?

A
  • Laburnum anagyroides
    (Golden chain)
    – Contains a nicotinic
    quinolizidine alkaloid, cytisine
32
Q

Imidazothiazoles (eg.
Levamisole) is sourced from?

A

Antiparasitic (antinematode,
microfilaricide) and immunostimulant

33
Q

What is Imidazothiazoles (eg. Levamisole) ADME?

A

Rapid oral absorption, metabolized in the
liver and excreted via urine and feces

34
Q

What is Imidazothiazoles (eg. Levamisole) MOT?

A
  • Acts as a nicotine-like ganglionic stimulant
    – Has both nicotinic and muscarinic effects
    – First there is stimulation, then blockade of
    ganglionic and skeletal muscle transmission
    Antiparasitic agent, (Anthelminthic, microfilaricide and immunostimulant).
    Has structural and functional similarity to nicotine
35
Q

What are the clinical signs of Imidazothiazoles (eg. Levamisole) toxicity’?

A
  • DUMBELS, anxiety, irritability, head
    shaking, lip-licking, muscle tremors,
    seizures, ataxia, hyperesthesia, clonic
    convulsions, CNS depression, behavioral
    changes, tachypnea, collapse and death due
    to respiratory failure
36
Q

What species are susceptible to of Imidazothiazoles (eg. Levamisole) toxicity’?

A

sheep, swine, cattle,
dogs, horse

37
Q

How do you treat Imidazothiazoles (eg. Levamisole) toxicity’?
What may be used to control some of the
cholinergic signs?

A
  • No antidote is available
  • Supportive and symptomatic therapy
    – Atropine may be used to control some of the cholinergic signs
38
Q

The other group of autonomic nervous system toxicants/toxins are those that
affect adrenergic transmission.
These affect receptors that are stimulated by norepinephrine and these receptors
are found in the CNS and sympathetic branch of the ANS.
Their effects are mediated by cAMP and phosphoinositol.

A
39
Q

Alpha receptors are located in which parts of the body?

A
40
Q

Beta receptors are located in which parts of the body?

A
41
Q

Epinephrine and Norepinephrine are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

alpha-Adrenergic-agonist
alpha non-specific
Anaphylaxis
Cardiac Arrest

42
Q

Phenylephrine and Methoxamine are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

alpha-Adrenergic-agonist
alpha-1-selective
Decongestants

43
Q

Clonidine are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

alpha-Adrenergic-agonist
alpha-2-selective
Hypertension, anxiety

44
Q

Epinephrine and Isoproterenol are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

Beta-Adrenergic-agonist
nonspecific

45
Q

Xamoterol, Dobutamine, and Prenalterol are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

beta-Adrenergic-agonist
beta-1-selective
Cardiogenic Shock

46
Q

Salbutamol, Formoterol, Terbutaline, Salmeterol, and Clenbuterol are what type of adrenergic receptors? Are they specific or non-specific? What are they used for?

A

beta-Adrenergic-agonist
beta-2-selective
Bronchodilators

47
Q

What is the ADME of bronchodilators?
MOT?

  • _______ and well-absorbed after ________ or ________
  • Metabolized in the ____ and excreted through _____ (70%) and _______ (10%)
  • Toxic dose: not determined. Adverse effects can occur at ________ dose
  • MOT: stimulation of _____ adrenergic receptors
A
  • Rapidly and well-absorbed after ingestion or
    inhalation
  • Metabolized in the liver and excreted
    through urine (70%) and feces (10%)
  • Toxic dose: not determined. Adverse effects
    can occur at therapeutic dose
  • MOT: stimulation of beta adrenergic receptors
48
Q

What are the clinical signs of Bronchodilator toxicity?

A
  • Peripheral vasodilation –> hypotension, bronchodilation, muscle tremors, increased heart rate and arrhythmias, hyperactivity, tachypnea, vomiting, hypokalemia, and death. May observe weakness and pulmonary edema.
49
Q

How do you treat bronchodilator toxicity?

A
50
Q

Pseudoephedrine, phenylephrine,
phenylpropanolamine, and ephedrine are all categorized as?

A

Decongestants

51
Q

What is the ADME of decongestants?

A

well-absorbed orally with rapid
onset of action

52
Q

What is the MOT of decongestants?

A

sympathomimetic
– Stimulation of α and β-adrenergic receptors

53
Q

What are the clinical signs of decongestant toxicity?

A
54
Q

How do you diagnose decongestant toxicity?

A
  • History and clinical signs
  • Detection of drug in plasma and urine
55
Q

How do you treeat decongestant toxicity?
1. What would you do in terms of decontamination?
2. How would you control the seizures
3. What else would you do?

A

See below

56
Q

What the brand names of Amitraz?

A

(BAAM, Ectodex, Mitaban, Point-Guard, Triatox)

57
Q

Amitraz should be used with caution in?

A

cats, puppies
Horses –> ileus

58
Q

Where can you source Amitraz from?

A
59
Q

How does an animal become exposed to Amitraz? What is its toxicity?

A
60
Q

What is the MOT of Alkitraz?

A
61
Q

What are the clinical signs of Alkitraz toxicity?
Chronic exposure results in?

A

See below

62
Q

How do you treat Alkitraz toxicity?

A
63
Q

List the alpha-adrenergic antagonists that are non-specific. What are they used for?

A

Phentolanine
Phenoxybenzamine
Hypertension

64
Q

List the alpha-adrenergic antagonists that are a1-selective. What are they used for?

A

Prazosin
Doxazocin
Tamulosin
Hypertension, urinary flow

65
Q

List the alpha-adrenergic antagonists that are a2-selective. What are they used for?

A

Yohimbine
Idazoxan

66
Q

List the beta-adrenergic antagonists that are non-specific. What are they used for?

A

– Propranolol
– Timolol
– Nadolol
– Pindolol
Angina, hypertension, dysrhythmias

67
Q

List the beta-adrenergic antagonists that are beta-1-selective. What are they used for?

A

– Metoprolol
– Acebutolol
– Atenolol
– Esmolol
Angina, hypertension, dysrhythmias

68
Q

List the beta-adrenergic antagonists that are beta-2-selective. What are they used for?

A

Butoxamine

69
Q

What is Sympatholytic Syndrome characterized by?

A

Vomiting, hyperventilation, convulsions,
hypotension, bradycardia or tachycardia, heart
block, arrhythmias, miosis, depression,
bronchoconstriction, lethargy, decreased/absent
bowel sounds

Toxicology (32 decks)

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