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

Exam 3- Ethylene Glycol-OTC medications Flashcards

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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
What samples need to be collected for diagnosis of Acetaminophen
Serum and whole blood -> clin path- hepatic damage, anemia (heinz bodies in cats) Liver and kidney -> histopathology
26
what liver lesions are associated with Acetaminophen?
Centrilobular to diffuse hepatic necrosis
27
What treatment is recommended for Acetaminophen?
Decontamination (induce emesis if necessary), Activated charcoal Antidote: N-Acetylcysteine Supportive treatment: antioxidant, RBCs (treatment of methemaglobin and anemia), Blood transfusion (coagulopathy)
28
What is the antedote for Acetaminophen?
N-Acetylcysteine
29
What is the active ingredient in Aspirin
Acetylsalicylic Acid
30
Can Aspirin be used in cats?
Yes! therapeutic levels are 10-25mg/kg/day | Toxic is much higher
31
MOA for Aspiring (Acetylsalicylic Acid)
Aspirin metabolized in the liver to metabolites Salicylate inhibits COX, decreased Prostacyclin, decreased Thromboxane. Uncoupling of oxidative Phosphorylation GI and Renal necrosis +/- Bleeding
32
Clinical Signs associated with Acetylsalicylic Acid
Predominately GI complications (anorexia, Vomiting, diarrhea and melena), Anuria, Muscle weakness, respiratory depression, CNS Depression
33
What samples and diagnostics are associated with Acetylsalicylic acid?
``` 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) ```
34
What lesions are associated with Aspirin
Gastric ulceration and perforation (GI bleeding), hepatic and renal necrosis
35
What treatments are associated with Aspirin
Decontaminate- emesis, AC, cathartics | Supportive: IV fluids, assisted ventilation, transfusions, Gastro protectants (Misoprostol, sucralfate, H2 blockers)
36
MOA for Ibuprofen
Metabolized in the liver and undergoes enterohepatic recirculation. Inhibition of COX Decreased prostaglandin (decreased blood flow, decreased epithelial function) GI and Renal Necrosis
37
Clinical Signs associated with Ibuprofen
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
What samples should you collect for Ibuprofen
Whole Blood, Serum, Urine, Kidney for histopathology Clinical Pathology: Metabolic acidosis, hepatic damage, secondary anemia due to blood loss, azotemia
39
What lesions are seen with Ibuprofen
GI: erosions, ulcerations, perforations, mucosal edema | Renal necrosis: papillary, cortical, coagulative with tubule dilation
40
treatment for Ibuprofen intoxication
No antidote Decontamination: Emesis, activated charcoal (repeated doses), cathartics Supportive care: IV fluids, Blood transfusions, Gastro protectants
41
what is | 5-Fluorouracil
Topical used for skin tumors in humans.
42
What is the toxic level of 5-Fluorouracil in canines
>43mg/kg is fatal. One dog punctured the tube without ingestion, and died Cats are more sensitive than dogs.
43
MOA of 5-Fluouracil
Inhibits RNA function, Tissue with high metabolic turnover affected
44
Clinical signs of 5-Fluouracil
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
Treatment of 5-Fluouracil
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
can you use Diazepam in cases of 5-FU intoxication?
No, it will be of little use
47
What is the MOA of tricyclic Antidepressents?
5-HT Reuptake inhibited NE reuptake inhibited- Hypotension Muscarinic binding of ACh inhibited. Anticholinergic effects Histamine Blocked- causing SEDATION
48
Clinical signs associated with TCAs
Small overdoses: Mild sedation, anorexia | Large overdose: Profound sedation, Cardiovascular collapse- leading cause of death
49
Treatment for TCA consumption
Decontamination- emesis, AC EKG-- monitor for widening of QRS, IVF 2x maintenance Control seizures: Diazepam/Benzodiazepines Physostigmine- Cholinesterase inhibitor
50
Serotonin Re-Uptake inhibitors MOA
5-HT reuptake inhibited Increase of 5-HT in synapse Development of SErotonin syndrome
51
Clinical Signs associated with SSRI's
CNS stimulation- excitation, tremors, seizures, Hyperthermia | GI: vomiting, Colic, Diarrhea
52
What samples should you collect for SSRI ingestion
Blood- detection of SSRI by GC/MS, Little help in interpreting degree of treatment necessary No lesion
53
Treatment of SSRI ingestion
``` Decontination: Emesis, AC Supportive: Phenobarbital- Seizures Cyproheptadine- 5-HT antagonist Cool IV fluids: Rehydrate and treat hyperthermia Antiemetics as needed ```
54
What is serotonin syndrome
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
Clinical Signs associated with Serotonin Synrome
``` CNS: Agitation, Vocalization GI: Vomiting Neuromuscular: Tremoring, Ataxia Hyperthermia Blindness ```
56
Toxicokinetics associated with Amphetamines
Rapid GI absorption Lipid soluble -> wide distribution: Brain Very little metabolism Excreted in the urine.
57
MOA for Amphetamines
Increased Catecholamine release | Decreased reuptake: NE, serotonin, Dopamine
58
Clinical signs of Amphetamines
Sympathomimetic: Mydriasis, CArdiac stimulant, CNS stimulant
59
What samples should be collected for Amphetamines?
Urine and stomach contects- detect the parent compound
60
What are recommended treatment methods for Amphetamines
No Antidote Decontaminate Supportive: Sedatives, IV fluids, Tachycardia, Tremors, Acidify Urine
61
What sample should you collect for Cocaine?
excreted in the urine Plasma, stomach contents Heart, and lung for Histopathology
62
MOA for Cocaine
Blocks Na+ channels -> conductance distrubances Increased catecholamine release: increased vasoconstriction Increased calcium in cardiac tissues increased contractility, increased O2 demand
63
Clinical Signs associated with Cocaine
Sympathomimetic- mydriasis Powerful CNS stimulant: Hyperesthesia, hyperactivity, erratic behavior, seizures Cardiotoxic**** Tachycardia, Arrhythmias, Hypertension -> Death
64
What are lesions associated with Cocaine
Pulmonary and cardiac hemorrhage | Pericardial edema
65
Treatment associated with Cocaine
No antidote Decontamination- Emesis and AC Control caradiac arrhythmias (B blocker - Propranolol) Control Seizures- Diazepam/Phenobarbital Respiratory support, control hyperthermia
66
Marijuana toxicokinetics
Rapid absorption (oral, inhalation) Metabolized in the liver Lipophilic- distributes to brain and fat Excreted in the bile
67
MOA of Marijuana
Acts on CBD receptors in the body- higher affinity than endogenous cannabinoids GABA release inhibited- Norepinephrine & serotonin release also affected
68
What samples should be collected for cases of Marijuana
SErum, urine, Stomach contents, Liver, kidney Source product
69
Clinical Signs associated with THC
``` CNS depressant Vomiting Euphoria -> Depression -> Coma Mydriasis Urinary incontinence (dribbling urine) ```
70
CBD clinical signs
``` Variable Asymptomatic in some cases Vomiting Depression: lethargy, ataxia Agitated ```
71
Clinical Signs associated with synthetic cannabinoids
``` Severe effect CNS stimulation Seizures/convulsions Ataxia Vomiting ```
72
Treatment for Marijuana cases
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
Where are opioids metabolized and excreted?
Metabolized in the liver, excreted in the urine
74
Clincial signs in DOGS and Opioids
Early excitation progressing to: respiratory depression, Death within 12 hours
75
Clinical signs in Cats and horses with Opioids
Excitation, aggression, seizures, mydriasis
76
What samples are needed to detect opioids
serum or urine
77
What are treatment methods associated with Opioids
``` 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
MOA of ethanol
Acts as an anesthetic agent by reversibly binding action potentials of neurons
79
Clinical Signs associated with Ethanol
Drowsiness/Depression Unconsciousness Respiratory and cardiac depression coma and even death
80
what samples are you evaluating to detect Ethanol?
Blood- BAC | Diagnosis is typically based on history of exposure
81
Treatment associated with Ethanol
early decontamination: emesis, gastric lavage, activated charcocal Supportive Care: respiratory support- maintain ventilation, respiratory stimulants, O2
82
MOA associated with Xylitol
Stimulates pancreatic secretion of insulin (dogs) | unknown: causes hepatic necrosis
83
Clinical Signs associated with Xylitol
Hypoglycemia (10-60min) secondary to hepatic necrosis: DIC, icterus, hemorrhage, melena, Diarrhea Loss of coordination and seizures
84
treatment associated with Xylitol
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
will Activated charcoal be effective in Xylitol cases
no- it has poor binding and little effect.

Toxicology (7 decks)

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