Toxicology Flashcards

1
Q

What are the 5 most common exposures for less than 5 yos

A
Cosmetic/personal care products
Household cleaning products
Analgesics
Foreign bodies/toys
Topical preparations
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2
Q

How do infants compare to adolescents in toxic exposures?

A
Easier to obtain exposure history
Typically presents within hours of exposure
More likely a non-toxic exposure
Typically, smaller amount ingested
Larger weight-based dose
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3
Q

When do we include pediatric toxic exposures to assessments?

A
Altered consciousness
Cardiac distress
Metabolic disturbances
Neurologic dysfunction
Pulmonary distress
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4
Q

What do we assess in cardiopulmonary distress?

A
HR
RR
BP
Temp
Skin tone
Skin color
Hydration status
Peripheral pulses
Perfusion
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5
Q

What is the antidote for Heparin?

A

Protamine

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6
Q

What is the antidote for Cyanide

A

sodium amyl nitrite/sodium thiosulfate

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7
Q

What is the antidote for TCAs and salicylates

A

Sodium bicarbonate

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8
Q

What is the antidote for warfarin

A

Vit K

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9
Q

What is the antidote for diphenhydramine

A

Benzos/sodium bicarbonate

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10
Q

What is the antidote for benzocaine

A

Methylene blue

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11
Q

What is the antidote for propranolol

A

Pressor support
Glucagon
Insulin
Dextrose

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12
Q

How is APAP metabolized

A
Glucoronidation (increases until age 3)
Sulfation
CYP450
Glutathione
Covalent binding - APAP-protein causes cell death
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13
Q

Antidote for APAP

A

N-acetylcysteine (NAC)

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14
Q

ADR of IV NAC

A

Anaphylactoid reaction

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15
Q

What is measured in metabolic disturbances in pediatric poisonings

A

Basic metabolic panel changes
Anion gap changes
Serum concentrations as warranted

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16
Q

Basic metabolic panel

A
Na
K
CO2
BUN
Scr
Glu
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17
Q

Anion gap equation

A

Na - [Cl + Co2]

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18
Q

What causes an elevated anion gap

A
M - Methanol
U - uremia
D - Diabetic ketoacidosis
P - Propylene glycol
I - Isoniazid, iron, infection
L - Lactic acidosis
E - Ethanol, ethylene glycol
S - Salcylates
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19
Q

Pediatric decontamination

A

Activated charcoal
Syrup of ipecac
Gastric lavage
Bowel irrigation

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20
Q

How does activated charcoal work in pediatric poisonings

A
High SA promoting absorption
Ionic binding and van der Waals forces bind toxins
Give = 1 hour post ingestion
10 activated charcoal per 1 toxin
Does not effectively absorb  EtOHs
0.5-2 g/kg in pediatric pts
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21
Q

How does syrup of ipecac work in poisonings

A

Stimulates chemoreceptor trigger zones

Vomiting occurs within 20 minutes

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22
Q

How does gastric lavage work in poisonings

A

10ml/kg warm water instilled and removed until contents are clear

23
Q

How does bowel irrigation work in poisonings

A

Pharmacologic stimulation of the GI tract
PEG and/or electrolyte flushes
For this to work it needs to be further down GI tract

24
Q

IV NAC administration

A

24 hour infusion

25
Q

IV NAC concentration issues

A

More free water (hyponatremia, seizures)

40 mg/ml

26
Q

Enteral NAC ADR

A

N/V/D

27
Q

Enteral NAC administration

A

72 hour regimen

28
Q

Ethylene glycol (where is it found, why is it ingested)

A

Engine coolant

Sweet taste

29
Q

What are the steps in metabolism of ethylene glycol

A

Ethylene glycol to glycoaldehyde via alcohol dehydrogenase
Glycoaldehydre to glycolic acid via aldehyde dehydrogenase
Glycolic acid to glycoxylic acid
Glycoxylic acid to oxalic acid

30
Q

ADRs of Ethylene glycol

A
< 5 hours
Ataxia
CNS depression
Coma 
Mental Status Change
31
Q

ADRs of glycolic acid

A

12-24 hours

Metabolic acidosis

32
Q

ADRs of glycoxylic acid

A
Metabolites
12-24 hours
CV collapse
CHF
Respiratory depression
Tachycardia
33
Q

ADRs of oxalic acid

A
1-3 days
ECG changes
Hypocalcemia
Nephrotoxicity
Tetany
34
Q

Supportive care of ethylene glycol poisonings

A

Thiamine (100 mg/d)

Pyridoxine (100 mg/d)

35
Q

Methanol locations

A

Solvents
Antifreeze
Fuels
Windshield wiper fluid

36
Q

Methanol supportive care

A

Folic or folinic acid 1 mg/kg q4-6h

37
Q

Methanol/ethylene glycol toxicity therapies

A

Ethanol
Fomepizole
Higher affinity for alcohol dehydrogenase than toxins (Fomepizole > ethanol)
Continue until toxin concentration < 25

38
Q

Ethanol administration

A
IV or enteral
IV requires central access
Goal serum concentration: 100-150
LD: 8ml/kg/h of 10% ethanol over 1 hour
MD: 0.8 mL/kg/h continuous infusion
39
Q

Ethanol ADRs

A
CNS depression
Hypoglycemia
Hyponatremia
Hypothermia
Respiratory depression
40
Q

Fomepizole MOA

A

Competitive alcohol dehydrogenase inhibitor

41
Q

Fomepizole advantages

A

No central access required
No mental status changes
No metabolic variations

42
Q

Fomepizole administration

A

LD: 15 mg/kg x 1, then 10 mg/kg q12h x 4
MD: 15 mg/kg q12h

43
Q

S/sx of toxic opioid exposures

A
Attention impairment
Coma
Constipation
Drowsiness
Loss of consciousness
Memory impairment
Nausea
Pupillary constriction
Respiratory depression
Over sedation
Slurred speech
44
Q

Naloxone/Naltrexone MOA

A

Pure opioid antagonist

Competitive inhibitor

45
Q

Naloxone dosing for toxic opioid exposures

A

= 20 kg: 0.1 mg/kg/dose
> 20 kg: 2 mg/dose
Every 2-3 minutes

46
Q

Naltrexone dosing

A

Titrate up once opioid free
Typical MD - 50 mg/d
Once daily dosing

47
Q

Antidote for organophosphates/carbamates

A

Atropine/pralidoxime

48
Q

Antidote for malignant hyperthermia caused by the disease process such as neuroleptic malignant syndrome or heat stroke; caused by drug toxicity such as from monoamine oxidase inhibitors or baclofen withdrawal

A

Dantrolene

49
Q

Antidote for iron

A

Deferoxamine

50
Q

Antidote for dig

A

digifab

51
Q

Antidote for benzos

A

Flumazenil

52
Q

Antidote for lead

A

Edetate calcium disodium (EDTA)
Dimercaprol
Succimer

53
Q

Antidote for methemoglobinemia

A

Methylene blue