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Toxicology > Unit 3 - Pharmaceuticals and Human Foods > Flashcards

Unit 3 - Pharmaceuticals and Human Foods Flashcards

1
Q

What were the top 2 pet toxins of 2019?

A

Over the counter medications and human prescription medications

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2
Q

What are the typical scenarios of OTC medication toxicosis?

A

Accidental ingestion, misuse, under the table dealings

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3
Q

What drug is tylenol?

A

Acetaminophen

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4
Q

What type of drug is tylenol?

A

analgesic and antipyretic

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5
Q

What is the most common source of tylenol posioning?

A

Purposeful use to treat the pet

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6
Q

T/F: There is no margin of safety with use of acetaminophen in cats, but there is a small one in dogs.

A

True

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7
Q

Where is acetaminophen absorbed? Metabolized? Secreted?

A

Absorbed in the GI tract

Metabolized in the liver

Secreted in the urine

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8
Q

What is the MOA of acetaminophen toxicosis?

A
  1. APAP metabolized to NAPQI: dogs conjugate & excrete, cats can’t conjugate
  2. Non-conjugated NAPQI binds to proteins & causes lipid peroxidation
  3. RBC lysis & hepatic necrosis
  4. Death
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9
Q

What enzyme do cats lack that don’t allow them to metabolize/excrete the toxic metabolite from acetaminophen metablolism (NAPQI)?

A

Glucuronosyltransferase

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10
Q

What clinical signs do cats exhibit with acetaminophen toxicosis?

A

Hematological effects - cyanosis (due to methemoglobinemia), hemolytic anemia, hematuria/ hemoglobinuria

**Metabolic (skin)** - **facial edema & swollen paws,** prurirtus
Hepatic complications (high dose) - encephalopathy, coagulopathy
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11
Q

What clinical signs do dogs exhibit with acetaminophen toxicosis?

A

GI - anorexia, nausea, vomiting, diarrhea

Hepatic associated - hemolysis, icterus

Hematological effects (high dose) - methemoglobinemia

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12
Q

How is acetaminophen toxicosis diagnosed?

A

Serum - ↑ APAP, Clin path
Whole blood - Clin path
Liver - histopath
Kidney - histopath
History of exposure

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13
Q

What clin path results are consistent with acetaminophen toxicosis?

A

↑ALT, ↑ AST, ↑ Bilirubin
↓ PCV w/ Heinz bodies- cats

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14
Q

What lesions are associated with acetaminophen toxicosis?

A

Centrilobular to diffuse hepatic necrosis

+/- renal tubular necrosis

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15
Q

How is acetaminophen toxicosis treated?

A

Antidote

Decontamination - induce emesis as necessary, activated charcoal, +/- cathartic

Antioxidant administration

RBCs or oxyglobin

Blood transfusion

Methylene blue - last resort

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16
Q

What is the antidote for acetaminophen toxicosis?

A

N-Acetylcysteine (Mucomyst) - needs to be administered immediately

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17
Q

What drug is aspirin?

A

Acetylsalicylic acid

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18
Q

What does aspirin do?

A

NSAID and anti-pyretic - COX inhibitor

Analgesic properties - osteoarthritis

Antithrombotic

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19
Q

T/F: Aspirin can be used therapeutically in cats.

A

True

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20
Q

Is the half-life of aspirin longer in cats or dogs?

A

Cats

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21
Q

Where is aspirin absorbed? Metabolized? Excreted?

A

Aborbed rapidly in GI tract

Metabolized in the liver

Excreted in the urine in a conjugated form

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22
Q

What is the MOA of aspirin toxicosis?

A
  1. Aspirin metabolized to metabolites
  2. Salicylate inhibits COX → ↓ Prostacyclin, ↓ Thromboxane, uncoupling of oxidative phosphorylation
  3. GI & renal necrosis +/- bleeding
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23
Q

When is the onset of clinical signs for aspirin toxicosis?

A

1 hour to days

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24
Q

What clinical signs are associated with aspirin toxicosis?

A

Predominantly GI
complications - anorexia, vomiting (+/- blood), diarrhea, melena
Anuria
Muscle weakness
Respiratory depression
CNS depression - coma, death

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25
Q

How is aspirin toxicosis diagnosed (samples and their purpose)?

A

Whole blood - clin path
Serum - clin path, aspirin
Urine - aspirin
Histopath - liver, kidney, stomach, & intestines

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26
Q

What clin path results are consistent with aspirin toxicosis?

A

↑ Anion gap - metabolic acidosis

↑ ALT, ↑ AST, ↑ Bilirubin - hepatic damage

↓ PCV - secondary anemia, blood loss

↑PT/PTT - loss of clotting factors & platelets

Azotemia - renal dysfunction

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27
Q

What lesions does aspirin toxicosis cause?

A

Gastric ulceration and perforation - gastric bleeding

Hepatic and renal necrosis

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28
Q

How is aspirin toxicosis treated?

A

Decontamination - emesis (if indicated), activated charcoal, cathartics

Supportive care - IV fluids (Na bicarb), assisted ventilation as needed, blood transfusions, GI protectants

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29
Q

What drugs are Advil and Motrin?

A

Ibuprofen

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30
Q

What type of drug is ibuprofen?

A

Analgesic, anti-inflammatory, and antipyretic

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31
Q

What is the most common source of ibuprofen poisoning?

A

Purposeful use to treat a pet

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32
Q

T/F: The toxic dose of ibuprofen is 1/2 in dogs than that in cats.

A

False - other way around

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33
Q

Where is ibuprofen absorbed? Metabolized? Excreted?

A

Rapidly absorbed in GI tract
Metabolized in liver
Excreted in urine

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34
Q

What is the MOA of ibuprofen toxicosis?

A
  1. Metabolized in liver
  2. Enters enterohepatic circulation
  3. Inhibits COX
  4. ↓ Prostaglandin → ↓blood flow, ↓ Epithelial flow
  5. GI & renal necrosis
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35
Q

What organ systems are targeted with ibuprofen toxicosis?

A

Gastrointestinal

Renal

Neurologic

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36
Q

When is the onset of GI clinical signs caused by ibuprofen toxicosis ? What are they?

A

Onset: 1-2 hrs

Anorexia, nausea, vomiting, abdominal pain, diarrhea, melena

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37
Q

When is the onset of renal clinical signs caused by ibuprofen toxicosis? What are they?

A

Onset: 12 hrs - 5 days

Oliguria, anuria, painful renal palpation, uremic breath

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38
Q

When is the onset of neurologic clinical signs caused by ibuprofen toxicosis? What are they?

A

Onset: 1-2 hrs

Depression, stupor, ↓ PLR, respiratory depression, coma

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39
Q

How is ibuprofen toxicosis diagnosed (samples and purpose)?

A

Whole blood - CBC

Serum - chemistry, ibuprofen levels

Urine - UA, renal baseline values

Histopath - kidney, stomach, intestines

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40
Q

What clin path results are consistent with ibuprofen toxicosis?

A

↑ Anion gap - metabolic acidosis

↑ALT, ↑ AST, ↑Bilirubin - hepatic damage

↓ PCV - secondary anemia, blood loss

Azotemia - renal dysfunction

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41
Q

What lesions are associated with ibuprofen toxicosis?

A

GI - erosions, ulcerations, perforations, and mucosal edema

Renal necrosis - papillary, cortical, and coagulative with tubule dilation

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42
Q

How is ibuprofen toxicosis treated?

A

Decontamination - emesis, activated charcoal, cathartics

Supportive care - IV fluids (Na bicarb), assisted ventilation, blood transfusions

Gastro protectants - Misoprostol, Sucralfate, H2 blockers, PPIs

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43
Q

How often should renal values be monitored in patients with ibuprofen toxicosis?

A

They should be monitored every 24 hours for 3 days

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44
Q

What is the common cause of 5-fluorouracil toxicosis in pets?

A

Accidenta consumption (it is an antineoplastic used for skin tumors)

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45
Q

T/F: 5-fluorouracil is an extremely toxic compound. Cats are more susceptible than dogs.

A

True

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46
Q

Where is 5-fluorouracil absorbed? Distributed?

A

Rapid absorption - oral, dermal

Wide distribution

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47
Q

What is the MOA of 5-Fluorouracil?

A

Inhibits RNA function

Tissue with high metabolic turnover affected

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48
Q

When is the onset of clinical signs due to 5-Fluorouracil toxicosis?

A

Rapid

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49
Q

What clinical signs are associated with 5-Fluorouracil toxicosis?

A

GI - bloody vomit, bloody diarrhea (GI sloughing)

CNS (30-45 mins) - Depression, tremors, seizures

Bone marrow suppression: Anemia, ↓ Immune system fx

Death in 7 hrs

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50
Q

How is 5-fluorouracil toxicosis diagnosed?

A

History of exposure and clinical signs

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51
Q

How is 5-fluorouracil toxicosis treated?

A

Decontamination ASAP (gastric lavage)

Seizure control - Phenobarbital (addn’l Propofol or pentobarbital)

IV fluids - maintain perfusion & hydration, colloids & blood products

GI protectants - H2 blockers, omeprazole

Broad spectrum abx

Bone marrow stimulation - Neupogen

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52
Q

For how long post 5-fluorouracil toxicosis should pateints be closely monitored?

A

For 4 weeks

53
Q

What TCAs are common antidepressents in toxicosis cases?

A

Amitriptyline (Elavil), Clomipramine, Desiparamine, Imipramine (Tofranil), and Nortriptyline

54
Q

What SSRIs are common toxicants?

A

Bupropion, Fluoxetine (Prozac), Paroxetine, Sertraline (Zolof), Trazadone

55
Q

What are the toxicokinetics for antidepressent toxicosis?

A

Rapid absorption

Protein bound

Metabolized in the liver

Wide volume of distribution

Excretion - bile (TCA) and urine (SSRi)

56
Q

What is the MOA of TCA toxicosis?

A

5-HT Reuptake inhibited

NE Reuptake inhibited - hypotension

Muscarinic binding of Ach inhibited - anticholinergic effects

Histamine blocked - sedation

57
Q

When is the onset of clinical signs for TCA toxicosis?

A

30 minutes

58
Q

What clinical signs are associated with small TCA overdoses?

A

Mild sedation and anorexia

59
Q

What clinical signs are associated with large overdoses of TCAs?

A

Histamine blockade - profound sedation

Alpha adrenergic blockade - Arrhythmias, tachycardia, CV collapse, hypotension

Anticholinergic effects - Mydriasis, dry mouth, tachycardia, urinary retention, ↓ GI motility

60
Q

What is the leading cause of death due to TCA toxicosis?

A

Cardiovascular collapse

61
Q

How is TCA toxicosis treated?

A

Decontamination - emesis, activated charcoal

EKG - monitor for widening QRS

IV fluids @ 1.5-2x maintenance

Control seizures - Diazepam/Benzo

Physostigmine (cholinesterase inhibitor)

62
Q

What is the MOA of SSRIs?

A

5-HT reuptake inhibited

Increase of 5-HT in synapse

Development of serotonin syndrome

63
Q

What clinical signs are associated with SSRI toxicosis?

A

CNS stimulation: excitation, tremors, seizures, hyperthermia

GI: vomiting, colic, diarrhea

64
Q

What samples are collected for the diagnosis of SSRI toxicosis?

A

Blood - detection by GC/MS

65
Q

What lesions are associated with SSRI toxicosis?

A

There are no lesions

66
Q

How is SSRI toxicosis diagnosed?

A

Detection of compound

Clinical signs

History of exposure/consumption

67
Q

How is SSRI toxicosis treated?

A

Decontamination - emesis, activated charcoal

Supportive care - Phenobarbital, cyproheptadine (5-HT antagonist), cool IV fluids, antiemetics

68
Q

What is serotonin syndrome?

A

Drug induced syndrome due to elevated serotonin levels in the CNS

69
Q

What are the contributing factors that may induce serotonin syndrome?

A

Decrease re-uptake of 5-HT

Increased synthesis

Decreased breakdown of 5-HT

5-HT agonists

70
Q

When is the onset of clinical signs associated with serotonin syndrome?

A

30 minutes to 12 hours

71
Q

What are the clinical signs of serotonin syndrome?

A

CNS - agitation, vocalization, confusion, seizures

GI - vomiting, abdominal pain, diarrhea, salivation

Neuromuscular - tremoring, ataxia

CV - tachycardia, hypertension

Hyperthermia

Blindness

72
Q

What are the toxicokinetics of amphetamines?

A

Rapid GI absorption

Wide distribution (lipid soluble) - liver, lung, kidney, brain

Very little metabolism

Excreted in the urine (acidic increases excretion)

73
Q

What is the MOA of amphetamines?

A

↑ Catecholamine release

↓ Reuptake - norepinephrine, serotonin, dopamine

74
Q

When is the onset of clinical signs for amphetamine toxicosis?

A

Minutes to hours

75
Q

What clinical signs are associated with amphetamine toxicosis?

A

Sympathomimetic - mydriasis

Cardiac stimulant - tachycardia, arrhythmias

CNS stimulant - hyperactivity, restlessness/ tremors, seizures, hyperthermia

76
Q

What samples are used for the diagnosis of amphetamine toxicosis?

A

Urine and stomach contents

77
Q

How is amphetamine toxicosis treated?

A

Decontaminate - emesis (w/in 15 minutes), activated charcoal

Supportive care:
Sedatives - phenobarbital, phenothiazine
IV fluids - tx hyperthermia, protect kidneys
Tachycardia - beta blockers
Tremors - methcarbamol
Acidify urine - ammonium chloride (↑ excretion)

78
Q

What sedative should not be used for the treatment of amphetamines?

79
Q

What are the toxicokinetics of cocaine?

A

Rapidly absorbed

Lipophilic - crosses BBB

Metabolized into metabolites….. (next question)

Excreted in the urine

80
Q

What are the metabolites of cocaine?

A

Benzoylecgonine

Ecgonine methyl ester

81
Q

What is the MOA of cocaine toxicosis?

A

Blocks Na channels - conductance disturbances

Increases catecholamine release - increases vasoconstriction

Increases calcium in cardiac tissue - increases cardiac contractility and thus O2 demand resulting in cardiac failure

82
Q

When is the onset of clinical signs for cocaine?

A

minutes to hours

83
Q

What clinical signs are associated with cocaine toxicosis?

A

Sympathomimetic - mydriasis

Powerful CNS stimulant - hyperesthesia, hyperactivity, erratic behavior, seizures

Cardiotoxic - tachycardia, arrhythmias, hypertension

84
Q

How is cocaine toxicosis diagnosed (sample and purpose)?

A

For detection of parent compound & metabolites - urine, plasma, stomach contents

For histopath - heart & lung

History of exposure

85
Q

What clin path abnormalities are consistent with cocaine toxicosis?

A

acidosis, hypoglycemia

86
Q

What lesions does cocaine toxicosis cause?

A

Pulmonary and cardiac hemorrhage

Pericardial edema

87
Q

How is cocaine toxicosis treated?

A

Decontamination - emesis & AC if possible

Control cardiac arrhythmias - beta blockers

Control seizures - Diazepam/ phenobarbitol

Respiratory support

Control hyperthermia

If necessary - careful removal of ingested bag

88
Q

What is the toxin of concern in marijuana?

A

Tetrahydrocannabinol (THC)

89
Q

What are the sources of THC?

A

Often mixed with chocolate
Baked goods
Plant material
Concentrated oils/products
CBD oil products
Synthetic cannabinoids (K2)

90
Q

Why do we have to be extra careful with CBD products?

A

Because concentrations can vary despite what the label says

91
Q

How is THC absorbed? Metabolized? Distributed? Excreted?

A

Rapid absorption - oral and inhalation

Metabolized in the liver

Distributed to brain and fat (lipophilic)

Excreted in bile

92
Q

What is the MOA of THC?

A

Acts on CBD receptors in the body

GABA release inhibited - dopamine secretion is uninhibited, euphoria
Norepinephrine & serotonin release also affected

93
Q

How is THC toxicosis diagnosed (samples and use)?

A

Gold standard- GC/MS or LC/MS
serum, urine, stomach contents, liver, kidney

94
Q

How is presence of CBD diagnosed?

A

CBD - GC flame ionization with source product

95
Q

T/F: The OTC human urine test is adequate for detection of THC in animals.

A

False - It can give false negatives

96
Q

When is the onset of clinical signs for THC/CBD/Cannabinoid toxicosis?

A

Minutes to hours

97
Q

What clinical signs are associated with THC toxicosis?

A

CNS depressant
Vomiting
Euphoria → Depression → Coma
Mydriasis
Urinary incontinence

98
Q

What clinical signs are associated with CBD toxicosis?

A

Variable C/S
Asymptomatic
Vomiting
Depression - lethargy, ataxia
Agitated

99
Q

What clinical signs are associated with synthetic cannabinoid toxicosis?

A

Severe effects:
CNS stimulation
seizures/ convulsions
Ataxia
Vomiting

100
Q

How is THC/CBD/Synthetic cannabinoid toxicosis treated?

A

Slow recovery - clinical effects may last for days

Decontamination - emesis, activated charcoal

Supportive - respiratory support & stimulation

Agitation & seizure control - butorphanol, diazepam, barbiturates

101
Q

What drug can be used to stimulate and provide respiratory support in patients with THC/CBD/Synthetic cannabinoid toxicosis?

102
Q

What are the opiods of concern for toxicosis?

A

Morphine, oxycodone, codeine, hydromorphone, fentanyl

Heroin, abused medications

103
Q

Opiod expsure is often due to what?

A

Accidental ingestion or inhalation (police dogs)

104
Q

Where are opiods absorbed? Distributed? Metabolized? Excreted?

A

Rapid absorption

Wide distribution (lipophilic) - crosses BBB

Metabolized in the liver

Excreted in the urine

105
Q

What opiods are full agonists?

A

morphine, codeine, heroin, fentanyl, meperidine

106
Q

What opiods are agonists/antagonists?

A

Butorphanol, Nalorphine

107
Q

What opiods are partial agonists?

A

Tramadol, buprenorphine

108
Q

What clinical signs are associated with opioid toxicosis in dogs?

A

Excitation early

Progression to depression/ stupor, respiratory depression, hypotension, coma,

Death w/in 12 hrs,

Miosis, vomiting, diarrhea, salivation, constipation

109
Q

What clinical signs are associated with opioid toxicosis in cats and horses?

A

Excitation
Aggression
Seizures
Mydriasis

110
Q

How are opioids detected?

A

In serum or urine

111
Q

What is the antidote for opioids?

A

Naloxone (Narcan)

112
Q

How is opioid toxicosis treated?

A

Naloxone

Decontamination - emesis, activated charcoal, fluids

Diazepam if seizing

Supportive care - artificial respiration

113
Q

What can be used in place of naloxone if it is not available?

A

Butorphanol - it is only a partial antagonist so it will not work as well

114
Q

What are the sources of ethanol for toxicosis cases?

A

Alcoholic beverages - wine, beer, liquor

Fermented foods - grains, fruits, bread dough

Commercial cleaning products - isopropyl alcohol

Fuel

115
Q

What are the toxicokinetics of ethanol toxicosis?

A

Rapid absorption - absorption slowed by food

Wide distribution

116
Q

What is the MOA of ethanol toxicosis?

A

Acts as an anesthetic agent by reversibly binding action potentials of neurons

117
Q

What clinical signs are associated with ethanol toxicosis?

A

Onset: W/in 1 hour

Behavioral changes -excitability, vocalizing, incontinence
Ataxia & incoordination
Vomiting
Drowsiness/ depression
Unconsciousness - loss of reflexes
Respiratory & cardiac depression
Coma
Death

118
Q

How is ethanol toxicosis diagnosed?

A

History of exposure/consumption, clinical signs, high BAC

119
Q

How is ethanol toxicosis treated?

A

Early decontamination - emetics (<15 min), gastric lavage, activated charcoal

Supportive care:
Respiratory support -maintain ventilation, respiratory stimulants, O2
Monitor & control acid/base balance (fluids w/ bicarbonate)
Yohimbine

120
Q

What are the sources of xylitol?

A

Chewing gum, mints, sweeteners, and various foods

121
Q

What are the toxicokinetics of xylitol?

A

Rapidly absorbed

Metabolized in liver

122
Q

What is the MOA of xylitol?

A

Stimulates pancreatic secretion of insulin

Unkown cause of hepatic necrosis

123
Q

What clinical signs are associated with xylitol toxicosis?

A

Vomiting

Hypoglycemia (10-60 mins) - weakness, depression, collapse, ataxia, tremoring/seizures

Secondary to hepatic necrosis (9-12 hrs) - DIC, icterus, hemorrhage, melena, diarrhea
Neurologic signs

124
Q

How is xylitol toxicosis diagnosed?

A

Blood glucose

Serum chemistry

Post mortem

125
Q

What blood glucose result is consistent with xylitol toxicosis?

A

Hypoglycemia

126
Q

What serum chemistry results are consistent with xylitol toxicosis?

A

Elevated hepatic enzymes - ALT, ALP, AST

Hyperbilirubinemia

Electrolyte abnormalities - hyper/hypophosphatemia, hypercalcemia

127
Q

What post mortem lesions are consistent with xylitol toxicosis?

A

Hepatic necrosis

Widespread icterus and hemorrhage

128
Q

How is xylitol toxicosis treated?

A

Decontamination - emesis & activated charcoal
IV crystalloid fluids - recommended even if initial BG is normal
Supportive hepatic care

Toxicology (32 decks)

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