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Toxicology > Exam 3- Ethylene Glycol-OTC medications > Flashcards

Exam 3- Ethylene Glycol-OTC medications Flashcards

1
Q

Do all antifreeze products contain toxic levels of Ethylene Glycol?

A

NO!

Propylene glycol does not have nay EG in it

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2
Q

Where is ethylene glycol metabolized?

A

Liver and kidneys
Oxalic acid binds calcium and deposits in the kidneys
Cats have a high baseline production of oxalic acid.
(lower lethal dose)

Excreted in the urine

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3
Q

Mechanism of action for Ethylene Glycol

A

Ethylene glycol is absorbed in the GI tract. In the liver it is metabolized by Alcohol Dehydrogenase. Glycolic Acid metabolized by Lactic dehydrogenase.
Acidosis occurs: Increased Osmolar gap, renal edema, and ulceration
Oxalic acid binds Ca. CaOxalate crystal deposition
Renal necrosis & Death

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4
Q

Clinical signs associated with Ethylene glycol

A

Initially- Drunken animal: vomiting, depression, PU/PD, ataxia
12-72hrs- Severe acidosis: Tachypnea, V, Dpression/Comatose, Bradycardia, Miosis, Seizures
>72hrs- Renal Failure: Oliguria ->Anuria, Oral ulcerations, Convulsions, Death

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5
Q

what samples are to be collected for ethylene glycol?

A

Ante mortem: Urine or serum

Post mortem: Kidney, Rumen contents

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6
Q

If you are not able to collect urine in a live patient with Ethylene glycol toxicity, what is the prognosis?

A

Poor!

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7
Q

What clinical pathology findings are consistent with Ethylene glycol?

A

Calcium oxalate crystalluria, Acidic urine, Azotemia, stress leukogram

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8
Q

What gross lesions and observations are associated with Ethylene glycol Intoxication?

A

Kidneys are pale, firm/congested +/- Pale streaks

Histopath is very telling: Block the light with a piece of paper (substitute to polarized lens)

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9
Q

On microscopic evaluation of the brain, what do you find with Ethylene Glycol toxicities

A

Deposition of crystals in vasculature.

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10
Q

What are the treatments associated with Ethylene Glycol?

A

Prevention of metabolsm is the goal
Diluted ethanol IV! (cheap, but side effects are possible)

Antidote: 4-metylprazole (extremely expensive)

Inhibits Alcohol dehydrogenase preventing the conversion of ethylene glycol to Glycoaldehyde

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11
Q

where do you find Methylxanthines

A

Coffee (caffeine), Theobromine (chocolate), Theophylline

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12
Q

What is a source for Theophylline?

A

Tea, human asthma medication, various foods and beverages

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13
Q

What toxicity is of concern with chocolate consumption?

A

Caffeine, AND Theobromine

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14
Q

How are Methylxanthines excreted?

A

Urine, Bile, and milk

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15
Q

Methylxanthines MOA

A

Competative antagonist of adenosine (Bronchodilation, Tachycardia, Vasoconstriction, CNS stimulation)
Increased intracellular calcium
Inhibiton of phosphodiesterase (increased cAMP -» Increased release of catecholamines
Stimulation of sympathetic Nervous system

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16
Q

Clinical Signs associated with Methylxanthine Toxicity

A 
CNS (hyperactivity, Agitation, Seizures)
Cardiac (tachycardia, arrhythmias)
Increased motor activity- Hyperexcitable, tremors
Polyuria
GI irritation- vomiting and diarrhea
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17
Q

What is the ideal sample for diagnostic testing associated with Methylxanthine toxicity?

A

GI content, serum, plasma, urine, milk

Lesions- no specific lesions, Evaluate oral cavity for the presence/odor of chocolate

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18
Q

what treatment is indicated for Methylxanthine Toxicity

A

Artificial respiration
Control seizures- Diazepam
Control arrhythmias: Lidocaine (dogs), Propranolol (Cats)
Decreased Blood Pressure- Metoprolol, Propranolol
Decontamination- Emesis, Gastric Lavage, Activated Charcoal

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19
Q

What is the drug in Tylenol?

A

Acetaminophen

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20
Q

can Acetaminophen be used in Cats?

A

Absolutely not. NO dose is safe

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21
Q

Why can’t cats have Acetaminophen?

A

Cats lack the enzyme glucluron L transferase. This prevents - not able to metabolize Acetaminophen to NAPQI

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22
Q

How is Acetaminophen broken down in dogs

A

Acetaminophen is broken down to NAPQI. It then binds to proteins and causes lipid peroxidation. RBC lysis & hepatic necrosis -> Death

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23
Q

Clincial Signs associated with Acetaminophen in CATS?

A

Hematological effects-> myoglobinemia, hemolytic anemia, hematuria
Metabolic effects - Facial edema and swollen paws
Hepatic complications at high doses- encephalopathy, coagulopathy

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24
Q

Clinical Signs associated with Acetaminophen in DOGS?

A

Gastrointestinal: anorexia, nausea, vomiting, diarrhea
Hepatic associated complications: hemolysis, icterus
Hematological effects at high doses

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25
Q

What samples need to be collected for diagnosis of Acetaminophen

A

Serum and whole blood -> clin path- hepatic damage, anemia (heinz bodies in cats)

Liver and kidney -> histopathology

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26
Q

what liver lesions are associated with Acetaminophen?

A

Centrilobular to diffuse hepatic necrosis

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27
Q

What treatment is recommended for Acetaminophen?

A

Decontamination (induce emesis if necessary), Activated charcoal

Antidote: N-Acetylcysteine

Supportive treatment: antioxidant, RBCs (treatment of methemaglobin and anemia), Blood transfusion (coagulopathy)

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28
Q

What is the antedote for Acetaminophen?

A

N-Acetylcysteine

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29
Q

What is the active ingredient in Aspirin

A

Acetylsalicylic Acid

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30
Q

Can Aspirin be used in cats?

A

Yes! therapeutic levels are 10-25mg/kg/day

Toxic is much higher

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31
Q

MOA for Aspiring (Acetylsalicylic Acid)

A

Aspirin metabolized in the liver to metabolites
Salicylate inhibits COX, decreased Prostacyclin, decreased Thromboxane. Uncoupling of oxidative Phosphorylation
GI and Renal necrosis +/- Bleeding

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32
Q

Clinical Signs associated with Acetylsalicylic Acid

A

Predominately GI complications (anorexia, Vomiting, diarrhea and melena), Anuria, Muscle weakness, respiratory depression, CNS Depression

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33
Q

What samples and diagnostics are associated with Acetylsalicylic acid?

A 
Whole blood (Metabolic acidosis, hepatic damage, decreased PCT increased PT/PTT, azotemia)
Serum, urine, and whole blood- detection of aspirin
Liver, kidney, stomach and intestines (histopath)
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34
Q

What lesions are associated with Aspirin

A

Gastric ulceration and perforation (GI bleeding), hepatic and renal necrosis

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35
Q

What treatments are associated with Aspirin

A

Decontaminate- emesis, AC, cathartics

Supportive: IV fluids, assisted ventilation, transfusions, Gastro protectants (Misoprostol, sucralfate, H2 blockers)

36
Q

MOA for Ibuprofen

A

Metabolized in the liver and undergoes enterohepatic recirculation.
Inhibition of COX
Decreased prostaglandin (decreased blood flow, decreased epithelial function)

GI and Renal Necrosis

37
Q

Clinical Signs associated with Ibuprofen

A

GI (1-2hrs)
Anorexia, nausea, vomiting, abdominal pain
Renal (12hrs-5 days)
Oliguria/anuria, painful renal palpation, uremic breath

Acute renal failure can occur in as little as 12 hours

38
Q

What samples should you collect for Ibuprofen

A

Whole Blood, Serum, Urine,

Kidney for histopathology

Clinical Pathology: Metabolic acidosis, hepatic damage, secondary anemia due to blood loss, azotemia

39
Q

What lesions are seen with Ibuprofen

A

GI: erosions, ulcerations, perforations, mucosal edema

Renal necrosis: papillary, cortical, coagulative with tubule dilation

40
Q

treatment for Ibuprofen intoxication

A

No antidote
Decontamination: Emesis, activated charcoal (repeated doses), cathartics
Supportive care: IV fluids, Blood transfusions, Gastro protectants

41
Q

what is

5-Fluorouracil

A

Topical used for skin tumors in humans.

42
Q

What is the toxic level of 5-Fluorouracil in canines

A

> 43mg/kg is fatal.
One dog punctured the tube without ingestion, and died

Cats are more sensitive than dogs.

43
Q

MOA of 5-Fluouracil

A

Inhibits RNA function, Tissue with high metabolic turnover affected

44
Q

Clinical signs of 5-Fluouracil

A

Rapid onset of signs
GI: bloody vomiting, diarrhea
CNS: Depression, tremors, seizures
Bone marrow suppression, anemia and decreased immune function

DEATH in 7 hours

45
Q

Treatment of 5-Fluouracil

A

Aggressive and heroic treatment required
Decontamination ASAP, limited capability due to rapid onset of clinical signs
Seizure control- Phenobarbital (4-16mg/kg IV)
IV fluids- maintain perfusion & hydration.

GI protectants- H2 blockers (Famotidine, Ranitidine, Omeprazole)
Broad spectrum antibiotics
Bone marrow suppression: Neupogen SQ every 3-5 days

46
Q

can you use Diazepam in cases of 5-FU intoxication?

A

No, it will be of little use

47
Q

What is the MOA of tricyclic Antidepressents?

A

5-HT Reuptake inhibited
NE reuptake inhibited- Hypotension
Muscarinic binding of ACh inhibited. Anticholinergic effects
Histamine Blocked- causing SEDATION

48
Q

Clinical signs associated with TCAs

A

Small overdoses: Mild sedation, anorexia

Large overdose: Profound sedation, Cardiovascular collapse- leading cause of death

49
Q

Treatment for TCA consumption

A

Decontamination- emesis, AC
EKG– monitor for widening of QRS, IVF 2x maintenance
Control seizures: Diazepam/Benzodiazepines
Physostigmine- Cholinesterase inhibitor

50
Q

Serotonin Re-Uptake inhibitors MOA

A

5-HT reuptake inhibited
Increase of 5-HT in synapse
Development of SErotonin syndrome

51
Q

Clinical Signs associated with SSRI’s

A

CNS stimulation- excitation, tremors, seizures, Hyperthermia

GI: vomiting, Colic, Diarrhea

52
Q

What samples should you collect for SSRI ingestion

A

Blood- detection of SSRI by GC/MS, Little help in interpreting degree of treatment necessary
No lesion

53
Q

Treatment of SSRI ingestion

A 
Decontination: Emesis, AC
Supportive: Phenobarbital- Seizures
Cyproheptadine- 5-HT antagonist
Cool IV fluids: Rehydrate and treat hyperthermia
Antiemetics as needed
54
Q

What is serotonin syndrome

A

Drug induced synrome due to elevated serotonin levels in the CNS- dogs are more susceptible than other species.

Contributing factors : Decreased re-uptake of 5-HT, increased synthesis, decreased breakdown of 5-HT.
LSD is a 5-HT antagonist

55
Q

Clinical Signs associated with Serotonin Synrome

A 
CNS: Agitation,  Vocalization
GI: Vomiting
Neuromuscular: Tremoring, Ataxia
Hyperthermia
Blindness
56
Q

Toxicokinetics associated with Amphetamines

A

Rapid GI absorption
Lipid soluble -> wide distribution: Brain
Very little metabolism
Excreted in the urine.

57
Q

MOA for Amphetamines

A

Increased Catecholamine release

Decreased reuptake: NE, serotonin, Dopamine

58
Q

Clinical signs of Amphetamines

A

Sympathomimetic: Mydriasis, CArdiac stimulant, CNS stimulant

59
Q

What samples should be collected for Amphetamines?

A

Urine and stomach contects- detect the parent compound

60
Q

What are recommended treatment methods for Amphetamines

A

No Antidote
Decontaminate
Supportive: Sedatives, IV fluids, Tachycardia, Tremors, Acidify Urine

61
Q

What sample should you collect for Cocaine?

A

excreted in the urine
Plasma, stomach contents
Heart, and lung for Histopathology

62
Q

MOA for Cocaine

A

Blocks Na+ channels -> conductance distrubances
Increased catecholamine release: increased vasoconstriction
Increased calcium in cardiac tissues
increased contractility, increased O2 demand

63
Q

Clinical Signs associated with Cocaine

A

Sympathomimetic- mydriasis
Powerful CNS stimulant: Hyperesthesia, hyperactivity, erratic behavior, seizures
Cardiotoxic** Tachycardia, Arrhythmias, Hypertension -> Death

64
Q

What are lesions associated with Cocaine

A

Pulmonary and cardiac hemorrhage

Pericardial edema

65
Q

Treatment associated with Cocaine

A

No antidote
Decontamination- Emesis and AC
Control caradiac arrhythmias (B blocker - Propranolol)
Control Seizures- Diazepam/Phenobarbital
Respiratory support, control hyperthermia

66
Q

Marijuana toxicokinetics

A

Rapid absorption (oral, inhalation)
Metabolized in the liver
Lipophilic- distributes to brain and fat
Excreted in the bile

67
Q

MOA of Marijuana

A

Acts on CBD receptors in the body- higher affinity than endogenous cannabinoids
GABA release inhibited-
Norepinephrine & serotonin release also affected

68
Q

What samples should be collected for cases of Marijuana

A

SErum, urine, Stomach contents, Liver, kidney

Source product

69
Q

Clinical Signs associated with THC

A 
CNS depressant
Vomiting
Euphoria -> Depression -> Coma
Mydriasis
Urinary incontinence (dribbling urine)
70
Q

CBD clinical signs

A 
Variable
Asymptomatic in some cases
Vomiting
Depression: lethargy, ataxia
Agitated
71
Q

Clinical Signs associated with synthetic cannabinoids

A 
Severe effect
CNS stimulation
Seizures/convulsions
Ataxia
Vomiting
72
Q

Treatment for Marijuana cases

A

No antidote associated with it
Slow recovery- clinical effects may last for days
Decontamination: emesis, AC
Supportive
**Respiratory support and stimulation-Doxapram
Agitation and seizure control: butorphanol, diazepam, barbiturates

73
Q

Where are opioids metabolized and excreted?

A

Metabolized in the liver, excreted in the urine

74
Q

Clincial signs in DOGS and Opioids

A

Early excitation progressing to: respiratory depression, Death within 12 hours

75
Q

Clinical signs in Cats and horses with Opioids

A

Excitation, aggression, seizures, mydriasis

76
Q

What samples are needed to detect opioids

A

serum or urine

77
Q

What are treatment methods associated with Opioids

A 
Naloxone -> reverse respiratory and CNS depression
    Reversal agent- full antagonist
    Butorphanol- PArtial antagonist
Decontamination- emesis, AC, fluids
Diazepam- control seizures if necessary
supportive Care- artificial respiration.
78
Q

MOA of ethanol

A

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

79
Q

Clinical Signs associated with Ethanol

A

Drowsiness/Depression
Unconsciousness
Respiratory and cardiac depression
coma and even death

80
Q

what samples are you evaluating to detect Ethanol?

A

Blood- BAC

Diagnosis is typically based on history of exposure

81
Q

Treatment associated with Ethanol

A

early decontamination: emesis, gastric lavage, activated charcocal
Supportive Care: respiratory support- maintain ventilation, respiratory stimulants, O2

82
Q

MOA associated with Xylitol

A

Stimulates pancreatic secretion of insulin (dogs)

unknown: causes hepatic necrosis

83
Q

Clinical Signs associated with Xylitol

A

Hypoglycemia (10-60min)
secondary to hepatic necrosis: DIC, icterus, hemorrhage, melena, Diarrhea

Loss of coordination and seizures

84
Q

treatment associated with Xylitol

A

No antidote
Decontamination: Emesis (contraindicated if hypoglycemic signs are present)
IV crystalloid fluids (with dextrose even if initial BG is normal)
Supportive hepatic care

85
Q

will Activated charcoal be effective in Xylitol cases

A

no- it has poor binding and little effect.

Toxicology (7 decks)

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