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
How is aspirin toxicosis diagnosed (samples and their purpose)?
Whole blood - clin path Serum - clin path, aspirin Urine - aspirin Histopath - liver, kidney, stomach, & intestines
26
What clin path results are consistent with aspirin toxicosis?
↑ Anion gap - metabolic acidosis ↑ ALT, ↑ AST, ↑ Bilirubin - hepatic damage ↓ PCV - secondary anemia, blood loss ↑PT/PTT - loss of clotting factors & platelets Azotemia - renal dysfunction
27
What lesions does aspirin toxicosis cause?
Gastric ulceration and perforation - gastric bleeding Hepatic and renal necrosis
28
How is aspirin toxicosis treated?
Decontamination - emesis (if indicated), activated charcoal, cathartics Supportive care - IV fluids (Na bicarb), assisted ventilation as needed, blood transfusions, GI protectants
29
What drugs are Advil and Motrin?
Ibuprofen
30
What type of drug is ibuprofen?
Analgesic, anti-inflammatory, and antipyretic
31
What is the most common source of ibuprofen poisoning?
Purposeful use to treat a pet
32
T/F: The toxic dose of ibuprofen is 1/2 in dogs than that in cats.
False - other way around
33
Where is ibuprofen absorbed? Metabolized? Excreted?
Rapidly absorbed in GI tract Metabolized in liver Excreted in urine
34
What is the MOA of ibuprofen toxicosis?
1. Metabolized in liver 2. Enters enterohepatic circulation 3. Inhibits COX 4. ↓ Prostaglandin → ↓blood flow, ↓ Epithelial flow 5. GI & renal necrosis
35
What organ systems are targeted with ibuprofen toxicosis?
Gastrointestinal Renal Neurologic
36
When is the onset of GI clinical signs caused by ibuprofen toxicosis ? What are they?
Onset: 1-2 hrs Anorexia, nausea, vomiting, abdominal pain, diarrhea, melena
37
When is the onset of renal clinical signs caused by ibuprofen toxicosis? What are they?
Onset: 12 hrs - 5 days Oliguria, anuria, painful renal palpation, uremic breath
38
When is the onset of neurologic clinical signs caused by ibuprofen toxicosis? What are they?
Onset: 1-2 hrs Depression, stupor, ↓ PLR, respiratory depression, coma
39
How is ibuprofen toxicosis diagnosed (samples and purpose)?
Whole blood - CBC Serum - chemistry, ibuprofen levels Urine - UA, renal baseline values Histopath - kidney, stomach, intestines
40
What clin path results are consistent with ibuprofen toxicosis?
↑ Anion gap - metabolic acidosis ↑ALT, ↑ AST, ↑Bilirubin - hepatic damage ↓ PCV - secondary anemia, blood loss Azotemia - renal dysfunction
41
What lesions are associated with ibuprofen toxicosis?
GI - erosions, ulcerations, perforations, and mucosal edema Renal necrosis - papillary, cortical, and coagulative with tubule dilation
42
How is ibuprofen toxicosis treated?
Decontamination - emesis, activated charcoal, cathartics Supportive care - IV fluids (Na bicarb), assisted ventilation, blood transfusions Gastro protectants - Misoprostol, Sucralfate, H2 blockers, PPIs
43
How often should renal values be monitored in patients with ibuprofen toxicosis?
They should be monitored every 24 hours for 3 days
44
What is the common cause of 5-fluorouracil toxicosis in pets?
Accidenta consumption (it is an antineoplastic used for skin tumors)
45
T/F: 5-fluorouracil is an extremely toxic compound. Cats are more susceptible than dogs.
True
46
Where is 5-fluorouracil absorbed? Distributed?
Rapid absorption - oral, dermal Wide distribution
47
What is the MOA of 5-Fluorouracil?
Inhibits RNA function Tissue with high metabolic turnover affected
48
When is the onset of clinical signs due to 5-Fluorouracil toxicosis?
Rapid
49
What clinical signs are associated with 5-Fluorouracil toxicosis?
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**
50
How is 5-fluorouracil toxicosis diagnosed?
History of exposure and clinical signs
51
How is 5-fluorouracil toxicosis treated?
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
52
For how long post 5-fluorouracil toxicosis should pateints be closely monitored?
For 4 weeks
53
What TCAs are common antidepressents in toxicosis cases?
Amitriptyline (Elavil), Clomipramine, Desiparamine, Imipramine (Tofranil), and Nortriptyline
54
What SSRIs are common toxicants?
Bupropion, Fluoxetine (Prozac), Paroxetine, Sertraline (Zolof), Trazadone
55
What are the toxicokinetics for antidepressent toxicosis?
Rapid absorption Protein bound Metabolized in the liver Wide volume of distribution Excretion - bile (TCA) and urine (SSRi)
56
What is the MOA of TCA toxicosis?
5-HT Reuptake inhibited NE Reuptake inhibited - hypotension Muscarinic binding of Ach inhibited - anticholinergic effects Histamine blocked - sedation
57
When is the onset of clinical signs for TCA toxicosis?
30 minutes
58
What clinical signs are associated with small TCA overdoses?
Mild sedation and anorexia
59
What clinical signs are associated with large overdoses of TCAs?
Histamine blockade - profound sedation Alpha adrenergic blockade - Arrhythmias, tachycardia, **CV collapse**, hypotension Anticholinergic effects - Mydriasis, dry mouth, tachycardia, urinary retention, ↓ GI motility
60
What is the leading cause of death due to TCA toxicosis?
Cardiovascular collapse
61
How is TCA toxicosis treated?
Decontamination - emesis, activated charcoal EKG - monitor for widening QRS IV fluids @ 1.5-2x maintenance Control seizures - Diazepam/Benzo Physostigmine (cholinesterase inhibitor)
62
What is the MOA of SSRIs?
5-HT reuptake inhibited Increase of 5-HT in synapse Development of serotonin syndrome
63
What clinical signs are associated with SSRI toxicosis?
**CNS stimulation:** excitation, tremors, seizures, hyperthermia **GI:** vomiting, colic, diarrhea
64
What samples are collected for the diagnosis of SSRI toxicosis?
Blood - detection by GC/MS
65
What lesions are associated with SSRI toxicosis?
There are no lesions
66
How is SSRI toxicosis diagnosed?
Detection of compound Clinical signs History of exposure/consumption
67
How is SSRI toxicosis treated?
Decontamination - emesis, activated charcoal Supportive care - Phenobarbital, cyproheptadine (5-HT antagonist), cool IV fluids, antiemetics
68
What is serotonin syndrome?
Drug induced syndrome due to elevated serotonin levels in the CNS
69
What are the contributing factors that may induce serotonin syndrome?
Decrease re-uptake of 5-HT Increased synthesis Decreased breakdown of 5-HT 5-HT agonists
70
When is the onset of clinical signs associated with serotonin syndrome?
30 minutes to 12 hours
71
What are the clinical signs of serotonin syndrome?
CNS - agitation, vocalization, confusion, seizures GI - vomiting, abdominal pain, diarrhea, salivation Neuromuscular - tremoring, ataxia CV - tachycardia, hypertension Hyperthermia Blindness
72
What are the toxicokinetics of amphetamines?
Rapid GI absorption Wide distribution (lipid soluble) - liver, lung, kidney, **brain** Very little metabolism Excreted in the urine (acidic increases excretion)
73
What is the MOA of amphetamines?
↑ Catecholamine release ↓ Reuptake - norepinephrine, serotonin, dopamine
74
When is the onset of clinical signs for amphetamine toxicosis?
Minutes to hours
75
What clinical signs are associated with amphetamine toxicosis?
Sympathomimetic - mydriasis Cardiac stimulant - tachycardia, arrhythmias CNS stimulant - hyperactivity, restlessness/ tremors, seizures, hyperthermia
76
What samples are used for the diagnosis of amphetamine toxicosis?
Urine and stomach contents
77
How is amphetamine toxicosis treated?
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
What sedative should not be used for the treatment of amphetamines?
Diazepam
79
What are the toxicokinetics of cocaine?
Rapidly absorbed Lipophilic - crosses BBB Metabolized into metabolites..... (next question) Excreted in the urine
80
What are the metabolites of cocaine?
Benzoylecgonine Ecgonine methyl ester
81
What is the MOA of cocaine toxicosis?
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
When is the onset of clinical signs for cocaine?
minutes to hours
83
What clinical signs are associated with cocaine toxicosis?
Sympathomimetic - mydriasis Powerful CNS stimulant - hyperesthesia, hyperactivity, erratic behavior, seizures **Cardiotoxic** - tachycardia, arrhythmias, hypertension
84
How is cocaine toxicosis diagnosed (sample and purpose)?
For detection of parent compound & metabolites - urine, plasma, stomach contents For histopath - heart & lung History of exposure
85
What clin path abnormalities are consistent with cocaine toxicosis?
acidosis, hypoglycemia
86
What lesions does cocaine toxicosis cause?
Pulmonary and cardiac hemorrhage Pericardial edema
87
How is cocaine toxicosis treated?
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
What is the toxin of concern in marijuana?
Tetrahydrocannabinol (THC)
89
What are the sources of THC?
Often mixed with chocolate Baked goods Plant material Concentrated oils/products CBD oil products Synthetic cannabinoids (K2)
90
Why do we have to be extra careful with CBD products?
Because concentrations can vary despite what the label says
91
How is THC absorbed? Metabolized? Distributed? Excreted?
Rapid absorption - oral and inhalation Metabolized in the liver Distributed to brain and fat (lipophilic) Excreted in bile
92
What is the MOA of THC?
Acts on CBD receptors in the body GABA release inhibited - dopamine secretion is uninhibited, euphoria Norepinephrine & serotonin release also affected
93
How is THC toxicosis diagnosed (samples and use)?
Gold standard- GC/MS or LC/MS serum, urine, stomach contents, liver, kidney
94
How is presence of CBD diagnosed?
CBD - GC flame ionization with source product
95
T/F: The OTC human urine test is adequate for detection of THC in animals.
False - It can give false negatives
96
When is the onset of clinical signs for THC/CBD/Cannabinoid toxicosis?
Minutes to hours
97
What clinical signs are associated with THC toxicosis?
CNS depressant Vomiting Euphoria → Depression → Coma Mydriasis Urinary incontinence
98
What clinical signs are associated with CBD toxicosis?
Variable C/S Asymptomatic Vomiting Depression - lethargy, ataxia Agitated
99
What clinical signs are associated with synthetic cannabinoid toxicosis?
Severe effects: CNS stimulation seizures/ convulsions Ataxia Vomiting
100
How is THC/CBD/Synthetic cannabinoid toxicosis treated?
Slow recovery - clinical effects may last for days Decontamination - emesis, activated charcoal Supportive - respiratory support & stimulation Agitation & seizure control - butorphanol, diazepam, barbiturates
101
What drug can be used to stimulate and provide respiratory support in patients with THC/CBD/Synthetic cannabinoid toxicosis?
Doxapram
102
What are the opiods of concern for toxicosis?
Morphine, oxycodone, codeine, hydromorphone, fentanyl Heroin, abused medications
103
Opiod expsure is often due to what?
Accidental ingestion or inhalation (police dogs)
104
Where are opiods absorbed? Distributed? Metabolized? Excreted?
Rapid absorption Wide distribution (lipophilic) - crosses BBB Metabolized in the liver Excreted in the urine
105
What opiods are full agonists?
morphine, codeine, heroin, fentanyl, meperidine
106
What opiods are agonists/antagonists?
Butorphanol, Nalorphine
107
What opiods are partial agonists?
Tramadol, buprenorphine
108
What clinical signs are associated with opioid toxicosis in dogs?
Excitation early Progression to depression/ stupor, respiratory depression, hypotension, coma, Death w/in 12 hrs, Miosis, vomiting, diarrhea, salivation, constipation
109
What clinical signs are associated with opioid toxicosis in cats and horses?
Excitation Aggression Seizures Mydriasis
110
How are opioids detected?
In serum or urine
111
What is the antidote for opioids?
Naloxone (Narcan)
112
How is opioid toxicosis treated?
Naloxone Decontamination - emesis, activated charcoal, fluids Diazepam if seizing Supportive care - **artificial respiration**
113
What can be used in place of naloxone if it is not available?
Butorphanol - it is only a partial antagonist so it will not work as well
114
What are the sources of ethanol for toxicosis cases?
**Alcoholic beverages -** wine, beer, liquor Fermented foods - grains, fruits, bread dough Commercial cleaning products - isopropyl alcohol Fuel
115
What are the toxicokinetics of ethanol toxicosis?
Rapid absorption - absorption slowed by food Wide distribution
116
What is the MOA of ethanol toxicosis?
Acts as an anesthetic agent by reversibly binding action potentials of neurons
117
What clinical signs are associated with ethanol toxicosis?
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
How is ethanol toxicosis diagnosed?
History of exposure/consumption, clinical signs, high BAC
119
How is ethanol toxicosis treated?
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
What are the sources of xylitol?
Chewing gum, mints, sweeteners, and various foods
121
What are the toxicokinetics of xylitol?
Rapidly absorbed Metabolized in liver
122
What is the MOA of xylitol?
Stimulates pancreatic secretion of insulin Unkown cause of hepatic necrosis
123
What clinical signs are associated with xylitol toxicosis?
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
How is xylitol toxicosis diagnosed?
Blood glucose Serum chemistry Post mortem
125
What blood glucose result is consistent with xylitol toxicosis?
Hypoglycemia
126
What serum chemistry results are consistent with xylitol toxicosis?
Elevated hepatic enzymes - ALT, ALP, AST Hyperbilirubinemia Electrolyte abnormalities - hyper/hypophosphatemia, hypercalcemia
127
What post mortem lesions are consistent with xylitol toxicosis?
Hepatic necrosis Widespread icterus and hemorrhage
128
How is xylitol toxicosis treated?
Decontamination - emesis & activated charcoal IV crystalloid fluids - recommended even if initial BG is normal Supportive hepatic care