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DWT Exam 3 > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What is toxicology?

A

The study of adverse effects of xenobiotic compounds, including chemical properties, bio effects, and treatments

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2
Q

Define a poison

A

Any substance capable of causing a deleterious response in a biological system

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3
Q

Define a toxin

A

A poisonous substance that is a specific product of the metabolic activities of a living organism

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4
Q

What factors determine toxicity? (5)

A
  1. Dose
  2. Duration/Frequency of exposure
  3. Route of exposure
  4. ADME
  5. Physiological factors
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5
Q

What is Bromethalin?

A

A rodenticide often sold as bait blocks, pellets, bars, and “worms”

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6
Q

How does Bromethalin become toxic?

A

It is absorbed and N-demethylated in the liver into Desmethylbromethalin. This form uncouples oxidative phosphorylation and disrupts Na+/K+ pumps leading to NEUROTOXICITY (edema and paralysis)

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7
Q

What happens during selenium deficiency?

A

Selenium deficiency can occur from feed mixing errors and deficient soil leading to white muscle disease, cardiomyopathy, and death

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8
Q

What happens during selenium toxicity?

A

Ingesting selenium accumulating plants and overdose can lead to lethargy, tachycardia, sweating, teeth grinding, hair loss, nail discoloration, hoof lesions, lameness, death

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9
Q

What happens during zinc deficiency?

A

Zinc deficient diets and genetic malabsorption can lead to alopecia and skin infections

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10
Q

What happens during zinc toxicity (pennies)

A

Ingestion of high zinc compounds can lead to intravascular hemolysis, GI irritation, hematuria, and hemoglobinuria

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11
Q

What defines acute exposure

A

Exposure to a chemical for less than 24 hours
Usually a single dose occurring from a single incident

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12
Q

What defines subacute exposure?

A

Exposure to a chemical for one month or less with REPEATED doses

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13
Q

What defines subchronic exposure?

A

Exposure to a chemical for 1-3 months with repeated doses

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14
Q

What defines chronic exposure?

A

Exposure to a chemical for 3 months to years with repeated doses

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15
Q

What are aflatoxins and what type of exposure do they usually cause?

A

Aflatoxins are produced by Aspergillus spp fungus in foods like corn that grow in hot, dry weather
Typically cause acute to subacute exposure

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16
Q

What is the mechanism of toxicity of Aflatoxin B1?

A

1) It can form DNA adducts in liver and lead to hepatocellular carcinoma
2) It can be conjugated to glutathione and be excreted
3) It can bind to hepatic proteins and lead to hepatotoxicity

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17
Q

What are the results of acute, subacute, and chronic aflatoxicosis?

A

Acute: massive liver damage, hemorrhage, death
Subacute: Liver damage, icterus, hemorrhagic enteritis
Chronic: hepatocellular carcinoma, cirrhosis

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18
Q

What are the 4 routes of exposure?

A
  1. Oral
  2. Dermal
  3. Inhalation
  4. Parenteral
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19
Q

What is the most common route of exposure in veterinary toxicology?

A

ORAL, almost all of the dose must pass through the liver

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20
Q

What is unique about inhalation toxicity?

A

Lungs have a large surface area and increased absorption
They avoid liver first pass effect and metabolism may occur in the lungs (BIRDS)

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21
Q

What are the clinical signs and pathologic findings of Teflon Fume Fever in birds?

A

Clinical signs: acute pulmonary distress and dyspnea, somnolence, convulsions, death

Necropsy: Acute, sever hemorrhagic pulmonary necrosis, edema

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22
Q

Why are birds more sensitive to gases than other companion animals?

A

They must have highly efficient gas exchange to deliver O2 to muscles during flight
They have a high metabolic rate, small size, and air is rapidly distributed to tissues

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23
Q

What are the four parenteral routes of administration?

A
  1. IV
  2. IP
  3. SQ
  4. IM
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24
Q

What does ADME stand for?

A

Absorption
Disposition
Metabolism
Excretion

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25
Q

What affects the absorption of a toxicant?

A

Lipid solubility of the neutral or non-ionized form of the drug
Lipophilic: organophosphate/carbamate insecticides
Insoluble salts: barium sulfate

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26
Q

How does pKa affect absorption?

A

The lower the pKa, the stronger the acid
Ionized compounds -> not passively absorbed, more water soluble
Un-ionized compounds -> passively absorbed, more lipid soluble

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27
Q

What differs between weak acids and weak bases in regards to absorption?

A

Weak acids are unionized in the stomach and diffuse through gastric mucosa. Unionized when pH < pKa

Weak bases are unionized and absorbed in the intestines . Unionized when pH > pKa

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28
Q

What happens when ruminants intake too much nitrate?

A

It’s converted to nitrite and exceeds microflora’s ability to reduce it. The nitrite is absorbed into blood and oxidize hemoglobin to Fe 3+. This leads to methemoglobin formation and O2 can’t reach tissues leading to vasodilation, methemoglobinemia, hypoxia, cyanosis

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29
Q

What are methods of preventing absorption?

A

Inducing emesis
Activated Charcoal with or without cathartic

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30
Q

What factors affect toxicant distribution

A
  1. Perfusion/blood flow through tissues ‘
  2. Protein binding of drug
    - acidic drugs bind protein -> low volume of distribution
    - basic drugs don’t bind protein and are extensively taken up by tissues -> larger volume of distribution
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31
Q

T/F poisons/drugs are not equally distributed through the body and tend to accumulate in specific tissues/fluids

A

true

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32
Q

What two things are less developed in younger animals leading to an increase in risk of toxicity?

A

Blood Brain Barrier
Gastrointestinal Tract
(increased risk of lead poisoning)

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33
Q

What pump is deficient in MDR-1 dogs leading to an increased risk of ivermectin toxicity?

A

P-glycoprotein

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34
Q

T/F The highest concentration of a toxin is always found in the target organ of toxicity

A

FALSE

35
Q

What organs does lead toxicity usually cause damage to?

A

Blood, liver, kidney, brain, bone (in order)

36
Q

What are the two phases of metabolism of toxins?

A

Phase I Rxn: Functionalization reactions
-convert xenobiotic to a more polar metabolite through hydrolysis, reduction, or oxidation

Phase II Rxn: Conjugation reactions
-conjugation of large, polar molecule to render xenobiotic hydrophilic for excretion

37
Q

What do phase I and II reactions have in common?

A

they both inactivate xenobiotic agents and can activate xenobiotic agent to pharmacologically active metabolite

38
Q

What is unique to Phase I reactions?

A

They may metabolize a xenobiotic agent to a toxic metabolite

39
Q

What can result from cats ingesting acetaminophen?

A

Cats have low levels of glucuronyltransferase, which leads to lipid peroxidation/RBC oxidation which leads to subsequent methemoglobinemia and hepatotoxicity and centrilobular necrosis

40
Q

T/F the route of excretion of the toxin can affect the degree of toxicosis in the animal

A

TRUE

41
Q

How can milk affect toxins?

A

Milk is slightly acidic and contains milk fat, this concentrates basic, fat soluble toxicants that can be passed to nursing animals

42
Q

What can result from white snakeroot poisoning?

A

leads to milk sickness in animals that drink the milk of animals ingesting white snakeroot. affected calves can develop muscle tremors and death

43
Q

What factors can affect excretion of toxins?

A

The rate can affect toxicity

Ion trapping: altering urine pH can inhibit reabsorption back into the blood stream

Principle: to “trap” the toxicants in its ionized form in the urine so it will be excreted. non-ionized can can diffuse across membranes, where ionized cannot

44
Q

What method can help increase excretion of methamphetamine (weak base)?

A

Administer ammonium chloride to acidify the urine to increase the percentage of ionized methamphetamine -> 70% excreted in urine

45
Q

How does chocolate cause toxicity?

A

Caffeine, theobromine, and theophylline inhibit adenosine and increase catecholamine release resulting in CNS stimulation -> tachycardia, diuresis, smooth muscle contraction, vasoconstriction, dopamine and glutamate release

46
Q

Why are dogs predisposed to chocolate toxicity?

A

the long half-life of theobromine
theobromine is metabolized into xanthine -> methyluric acid by hepatic CYP 450

47
Q

What are the clinical signs and treatment options for chocolate toxicity?

A

Clinical signs: tachycardia, hypertension, hyperactivity, CNS excitability, muscle tremors, V/D, tachypnea, respiratory failure, may last for 1-3 days

Treatment: Beta-blockers, lidocaine, atropine, emesis induction, activated charcoal, gastric lavage, anticonvulsants

48
Q

Why do older animals typically have a longer half life of xenobiotics?

A

Decreased metabolic capacity and decreased kidney function

49
Q

How does pregnancy and lactation affect toxicity?

A

hormone changes can alter metabolism
circulatory changes alter distribution
fetus has increased susceptibility
fat soluble chemicals may be excreted in milk

50
Q

What causes an adverse drug reaction?

A

An over-accumulation of the drug in the animal
In-flow exceeds out-go
1) Decreased ability to eliminate
2) Altered metabolism
3) Selective organ uptake

51
Q

What is an adverse drug reaction?

A

Any toxic or unintended response to a drug that occurs at appropriate therapeutic doses

52
Q

What are macrolide endectocides and what are they commonly used for?

A

Avermectins and Milbemycins
ex. heartgard, sentinel, trifexis

Typically used as an amtihelmintic and heart worm preventative
(Injection, PO liquid/tablets, pour ons, topical drops)

53
Q

What gene are some collies deficient in leading to an increased risk of ivermectin sensitivity?

A

MDR1 gene -> P glycoprotein cannot efficiently prevent ivermectin and moxidectin from crossing the BBB

54
Q

What is the mechanism of action of the macrolide endectocides?

A

They bind glutamate receptors on chloride channels in the cell membrane of neurons in parasites which leads to an increase in cell permeability and muscle paralysis.

GABA AGONISTS in MDR-1 deficient animals

55
Q

What are clinical signs of Macrolide Endectocides toxicity?

A

-Ataxia
-Depression, disorientation
-Bradycardia
-Hypersalivation
-Mydriasis
-V/D
-Tremors, seizures

56
Q

What can cause a non-toxic adverse drug reaction?

A

Corticosteroids in dogs -> PU/PD
Partial inhibition of ADH secretion

57
Q

Can non toxic adverse drug reactions be beneficial? List an example

A

Yes
Diphenhydramine is typically used as an antihistamine for allergy treatment, but can cause a sedative effect (sleep aid, anxiolytic) by acting as a mild inhibitor of serotonin reuptake.

58
Q

What are common features of idiosyncratic adverse drug reactions?

A

-usually vary between individuals and occurs in animals at therapeutic conditions
-HOST DEPENDENT
-They are rare and unpredictable
-Dependent on CHEMICAL PROPERTIES, not pharmacologic
-Occur within 1-2 months of treatment and hepatotoxicity is most commonly reported

59
Q

What are the proposed mechanisms of idiosyncratic adverse drug reactions?

A

1) Metabolic activation of a drug to reactive metabolites
-> covalent bonding of hepatocellular macromolecules -> hepatotoxicity
2) Immune Mediated Toxicity
-> drug or reactive molecule + biomolecule -> cellular damage and immune system activation
-> drug or reactive metabolite -> sensitizes immune system to drug and causes an immune response

60
Q

Define antagonism in its relation to drug interactions and list the different types

A

Antagonism is an interaction between two or more drugs that have opposite effects on the body
This may be exploited in toxicology and medicine

Types: Functional, chemical, dispositional, receptor

61
Q

Define functional antagonism

A

An interaction between two or more drugs that produce opposite effects on the same physiological function

Treating the clinical signs observed

62
Q

What is Strychnine? List the mechanism of toxicity and treatment available

A

Strychnine is an alkaloid toxin from Strychnos nux-vomica plant

Mechanism of toxicity: blocks the inhibitory neurotransmitter glycine leading to CNS stimulation
-> excess sensory input and exaggerated responses and rigor, sardonic “grin” from facial muscle spasms, seizures, convulsions

Treatment: Methocarbamol, pentobarbital, propofol

63
Q

Define chemical antagonism

A

A chemical interaction that occurs between two drugs that produces a less toxic product
(chelation therapy and heavy metal toxicity)

64
Q

T/F Lead is 97-99% bound to hemoglobin in the blood

A

True, this allows it to reach the liver, brain, kidney, and bone

65
Q

What is the goal of chelation therapy?

A

To give a drug that chemically binds the toxic metal in order to form a less toxic complex for excretion

66
Q

Define dispositional antagonism

A

Alteration of absorption, distribution, or excretion of a poison or drug such that the concentration or duration of time the poison or drug is at the target organ is diminished

(apomorphine, activated charcoal +/- cathartic)

67
Q

Define receptor antagonism

A

Two chemicals that bind the same receptor producing less toxicity than when given separately

“blockers” naloxone competes with morphine like drugs

68
Q

What is the mechanism of action of opiates and opioids?

A

Inhibit neurotransmitter release in response to pain stimulus decreasing neuron excitation resulting in ANALGESIA

69
Q

What opioid receptor does naloxone bind the strongest to?

A

The Mu receptor

70
Q

What are pyrethrins/pyrethroids

A

Insecticide
Pyrethrins: derived from chrysanthemum flowers
Pyrethroids: synthetic analogues with greater stability and potency
Generally safe for mammals as they are more selective for insects than mammals

71
Q

What is the mechanism of toxicity for pyrethrins/pyrethroids?

A

They bind to voltage-dependent sodium channels in neurons causing prolonged Na+ influx into neurons
This leads to hyper excitability of cells and depolarization of neurons
TWO TYPES

72
Q

What are the two types of pyrethrin/pyrethroid toxicity?

A

Type I: No alpha-cyano group
Pyrethrin, permethrin, allethrin, resmethrin, phenothrin
Prolonged depolarizing action potential -> repetitive neuron firing and nervous system stimulation

Type II: Has an alpha-cyano group
deltamethrin, fenvalerate, cyfluthrin
Suppression of action potential and reduced ability of nerve to fire -> longer duration of action

73
Q

What syndrome results from Type I pyrethrin/pyrethroid toxicity?

A

T (tremor) SYNDROME
-progressive body
-hyperexcitability
-exaggerated startle response
-prostration

74
Q

What syndrome results from Type II pyrethrin/pyrethroid toxicity?

A

CS (Choreoathetosis/salivation syndrome)
-hypersalivation
-weakness
-irregular contractions
-ataxia
-tonic seizures

75
Q

T/F Cats aren’t very sensitive to concentrated pyrethrin products

A

FALSE
Cats can have depression, anorexia, vomiting, hyper salivation, facial twitching, hyperthermia, and death if products meant for dogs get on cats

76
Q

What are different treatments for pyrethrin/pyrethroid toxicity?

A

Ingestion: If no symptoms, then induce vomiting or give activated charcoal

Allergic skin reaction: bathe in warm water and liquid dish detergent, topical vitamin E, diphenhydramine

Tremors/Seizures: methocarbamol, phenobarbital, midazolam, propofol

Symptomatic/Supportive care: fluid therapy and hydration

77
Q

What animals are most sensitive to pyrethrin/pyrethroid toxicity?

A

Fish, reptiles, cats

78
Q

What are common causes of insecticide poisoning in animals?

A

Malicious intent, accidental exposure, misuse or overuse of product

79
Q

What is the mechanism of toxicity of organophosphates and carbamate?

A

They both inhibit the enzyme acetylcholinesterase, leading to a buildup of acetylcholine at the neuromuscular junction
This leads to excessive stimulation of muscarinic, nicotinic, and CNS cholinergic receptors

80
Q

What are the muscarinic signs of organophosphate and carbamate toxicity?

A

Parasympathetic overstimulation
SLUDDE signs
Salivation
Lacrimation
Urination
Defecation
Dyspenia
Emesis

81
Q

What are the nicotinic signs of organophosphate and carbamate toxicity?

A

Stimulatory phase: muscle fasciculations and tremors, muscle stiffness

After stimulatory phase: flaccid paralysis -> weakness due to muscle fatigue

CNS signs: restlessness, ataxia, confusion, depression

82
Q

What causes death from organophosphate and carbamate toxicity?

A

The inhibition of medullar respiratory center in CNS
excessive bronchial secretions
bronchoconstriction
paralysis of diaphragm

Respiratory failure as a result of nicotinic receptor blockage and airway obstruction by copious amounts of respiratory secretions and bronchocontriction

83
Q

What is the treatment for muscarinic signs of organophosphate and carbamate toxicity?

A

Atropine Sulfate
No affect on nicotinic receptors

DWT Exam 3 (6 decks)

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