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DWT exam 3 > Toxicology adverse drug effects and case management > Flashcards

Toxicology adverse drug effects and case management Flashcards

1
Q

adverse drug reaction

A

Reactions occurring due to over-accumulation of the drug in the animal
“In-flow exceeds out-go”
ex: decreased ability to eliminate, altered metabolism, selective organ uptake
Any toxic or unintended response to a drug that occurs at appropriate therapeutic doses

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2
Q

Macrolide Endectocides adverse effects

A

TOXIC
Some collies are deficient in multi-drug resistance gene (MDR1)
act as GABA agonists when they bind receptor in MDR-1 deficient animals
Clinical Signs:
* Ataxia
* Behavioral changes
* Depressed, disoriented
* Bradycardia
* Hypersalivation
* Mydriasis
* Vomiting, diarrhea
* Tremors, seizures

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3
Q

Non toxic adverse reaction example

A

Corticosteroids given to dogs = PU/PD
* Others: THC, benzodiazepines, barbiturates

Partial inhibition of antidiuretic hormone (vasopressin) secretion

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4
Q

beneficial/therapeutic reaction example

A

Diphenhydramine

Antihistamine for allergy treatment
* Inverse agonist of histamine H1 receptor
* Binds same receptor as histamine

Sedative Effect (sleep aid, anxiolytic)
* Mild inhibitor of reuptake of serotonin
* Crosses blood-brain barrier antagonizing central H1 receptors

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5
Q

idiosynchratic adverse drug reactions

A

“Unique” or unusual – individual

Occurs in animals at therapeutic concentrations

Host-dependent, not dose-dependent

Rarely occur (< 0.1%) and are unpredictable

Dependent on chemical properties of drug, not pharmacological properties

Occurs within 1 to 2 months of drug therapy

Idiosyncratic hepatotoxicity more commonly reported

ex: carprofen hepatotoxicity 14-30 days during treatment

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6
Q

functional antagonism

A

An interaction between two or more drugs (or drugs + poison) that produce opposite effects on the same physiological function
Treating the clinical signs observed
ex: Strychnine
* inhibit glycine (inhibitory)
* causes: Excess sensory input & exaggerated responses, rigor, Sardonic “grin” – sustained facial muscle spasms, Seizures, convulsions
* treatment: calm NS (propofol)

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7
Q

chemical antagonism

A

A chemical interaction (reaction) that occurs between two drugs (or drug + poison) that produces a less toxic product

ex: Chelation therapy and heavy metal toxicity
ex: antivenom

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8
Q

chelation therapy

A

chemical antagonism
Chelation therapy and heavy metal toxicity
* 99% of lead is bound to hemoglobin (does not show up in serum)
* Goal: give a drug that chemically binds to the toxic metal in order to form a less toxic complex (chelation drug + toxic metal) for excretion
* levels in blood may go up first (pulls toxic metal out of bone, blood)

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9
Q

antivenom

A

chemical antagonism
Anti-venom – antibodies against venom

Given to counteract envenomation by poisonous snakes

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10
Q

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

Absorption
* Administration of activated charcoal/cathartic
* Apomorphine

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11
Q

Activated charcol treatment

A

Dispositional Antagonism: Preventing Toxicant Absorption
“Activated” = petroleum or vegetable origin, not mineral/animal
Absorbs toxin/toxicant in GI tract > fecal excretion
Decreases systemic absorption
Implement immediately for maximal adsorption to poison

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12
Q

Receptor Antagonism

A

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

ex: “blockers” = Naloxone competes with morphine-like drugs for same receptor

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13
Q

Stabilizing a poisoned patient

A

Airway/Breathing
* ex: tachypnea, bronchospasm

Circulation
* assess mucus membranes, BP, temp, HR

Disability/defects
* pupillary light reflex, mental statusm ambulation, GI

ABCD

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14
Q

Oral exposure decontamination

A
  1. Emesis
  2. Activated Charcoal
  3. Gastric Lavage
  4. Endoscopy/surgery
  5. Lipid Emulsion Therapy
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15
Q

ingestion of corrosive agents

A

dilute with milk or water
DO NOT INDUCE VOMITING

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16
Q

apomorphine

A

Emetic activity = stimulating dopamine receptors
Given parenterally (IM or IV) or topically in the conjunctival sac
Triggers CRTZ = vomiting
Preferred emetic drug for dogs

Side effects:
* CNS and respiratory depression, protracted vomiting
* Sedative side effects reversed with naloxone, does not stop vomiting

17
Q

Clevor® (Ropinirole)

A

Ophthalmic solution for emesis in dogs
Dopamine agonist
Drops depend on body weight
5.1 – 10 kg = 3 drops in one eye
20.1 – 35 kg = 4 drops in one eye

18
Q

Treatment for vomiting (protractive vomiting)

A
  • Cerenia (Maropitant) – blocks neurotransmitter involved in emesis
  • Reglan (Metoclopramide) – increases GI muscle contractions
19
Q

Hydrogen Peroxide (3% H2O2)

A

** Dogs**

“Currently” recommended for at-home emesis induction in dogs…only 3% used. Higher concentrations = severe gastritis

Induces emesis by causing direct, gastric irritation (≈ 10 min)

1 to 5 mL/kg bwt (do not exceed 50 mL in dogs)
Client-based measurement = 5 mL = 1 teaspoon

Ineffective in cats – hemorrhagic gastritis
Froth and foam at mouth and sometimes don’t vomit
Burns usually noted on arrival at clinic

20
Q

emetic agents in cats

A

Xylazine (Rompun®, Anased®)
Dexmedetomidine (Precedex™)
Emetic activity = stimulates α2-adrenergic receptors and vomiting center

Cats: Considered emetics of choice; 0.44 mg/kg IM
Dogs: 1.1 mg/kg SC or IM

Side effects: CNS and respiratory depression, bradycardia, hypotension

Side effects reversed with yohimbine

21
Q

When to induce vomiting

A

Usually induce <1hr after ingestion
asymptomatic patient
Can induce ≤ 6 hours
* Grapes, raisins
* Xylitol
* Massive ingestions
* Chocolate
* Bezoars

Drugs that decrease gastric emptying (longer window):
* Opioids
* Anticholinergics
* Tricyclic antidepressants
* Salicylates

22
Q

Contraindications for Emesis Induction

A

Patient is symptomatic

Laryngeal paralysis

Megaesophagus

Risk of aspiration pneumonia
* Brachycephalic breeds (Bulldogs, Boston Terriers)
* Ingestion of hydrocarbons (Petroleum products, Gasoline, Kerosene, Motor oil)
* < 3 months old

Ingestion of corrosive agents (Batteries, Toilet bowl or drain cleaners, Oven cleaners)

Patient is seizing

Rodents, horses, ruminants, rabbits

23
Q

activated charcol

A

“Activated” = petroleum or vegetable origin, not mineral/animal
Adsorbs toxin/toxicant in GI tract > fecal excretion
* Decreases systemic absorption

Effective for toxicants that undergo enterohepatic recirculation

may contain cathartics

24
Q

Cathartics

A

Sorbitol
* Poorly absorbable salts that osmotically draw water into the gut lumen > stimulate movement enhancing elimination of activated charcoal

Large Animals:
* Magnesium sulfate and sodium sulfate are used as cathartics
* Sorbitol can also be used as a laxative/cathartic

25
Q

What does NOT bind charcol?

A

Alcohols
* Ethylene glycol
* Ethanol

Xylitol

Heavy metals

Nitrates, nitrites, chlorates

26
Q

contraindications for activated charcol

A

Late-stage presentation
Hypernatremia
Hypovolemic shock
Compromised airway
GI obstruction
Risk of aspiration pneumonia
* Caustic substance
* Hydrocarbon

Vomiting animal
Lack of borborygmi

27
Q

gastric lavage

A

May be more effective than emesis at removing gastric contents
Requires prep, IV catheter, sedation, intubation, endotracheal insufflation, flush with 5-10 mL/kg warm water, agitate stomach, aspirate contents, pump stomach

When?
* Ingestion of deadly medications/life-threatening situations
* Beta-blockers, metaldehyde, calcium-channel blockers
* Unsuccessful emesis
* Species that cannot vomit
* Symptomatic patients with large ingestion

28
Q

gastric lavage contraindications and risks

A

Contraindications
* Ingestion of hydrocarbons or corrosives
* Recent surgery
* Patient unstable

Risks
* Aspiration pneumonia
* Esophageal/gastric rupture
* Electrolyte imbalances

29
Q

lipid emulsion therapy

A

Typically soybean oil
Creates a lipid “sink” in the blood > lipid binds highly lipid soluble toxicants

Given IV as a bolus dose at 1.5 mL/kg (20% lipid emulsion)
* Followed by infusion at 0.25 mL/kg/minute for 30-60 minutes)
* Repeat if blood not lipid-filled in PCV tube
* See lipid layer at about 1-2% of volume

Monitor vitals

Case reports:
* Macrolide endectocide overdose
* Baclofen
* NSAIDs
* Marijuana
* Tremorigenic mycotoxins

30
Q

What samples to collect antemortem?

A
  • Vomitus (all available)
  • Urine (all available)
  • Whole blood (5 mL in red top clot tube)
  • Whole blood (5 mL in purple top EDTA tube)
  • Serum
  • Source material – water, food, suspect foodstuff, bait
  • Hair or fur (if dermal exposure)
31
Q

What samples to collect antemortem?

A
  • Vomitus (all available)
  • Urine (all available)
  • Whole blood (5 mL in red top clot tube)
  • Whole blood (5 mL in purple top EDTA tube)
  • Serum
  • Source material – water, food, suspect foodstuff, bait
  • Hair or fur (if dermal exposure)
32
Q

What samples to collect postmortem?

A
  • Liver
  • Stomach contents
  • Brain (1/2)
  • Kidney (1/2)
  • Urine
  • Eyeball or ocular fluid
  • Any source material (Water, food, suspect foodstuff, bait)

Fix representative tissues in 10% formalin
Save samples for bacteriology and virology

33
Q

What samples to collect postmortem?

A
  • Liver
  • Stomach contents
  • Brain (1/2)
  • Kidney (1/2)
  • Urine
  • Eyeball or ocular fluid
  • Any source material (Water, food, suspect foodstuff, bait)

Fix representative tissues in 10% formalin
Save samples for bacteriology and virology

34
Q

Qualitative test

A

Positive or Negative
* No concentrations given
* Ethylene glycol
* Cyanide
* Colorimetric tests

35
Q

quantitative test

A

Concentrations of drug, toxin, or toxicant are calculated (quantitated)

Usually report in units of:
* ppb = parts per billion
* ppm = parts per million

36
Q

ppb vs ppm

A

1,000 ppb = 1 ppm

1 ppm =
* 1 mg/L
* 1 µg/g
* 1,000 ppb
* 10,000%

1 ppb =
* 1 µg/L
* 1 ng/g
* 0.001 ppm
* 0.0000001%

DWT exam 3 (14 decks)

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