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Emergency Med > Toxicology > Flashcards

Toxicology Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

General assessment

A 
Hx of ingestion/inhalation should try to be obtained
-Time 
-Amount
-Pill bottles found
Physical exam
-CC/symptom may suggest the dx
Toxicology lab assessment
-Platelets, CMP, drug screen, EtOH level
Look for anything on children's clothes
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2
Q

Gastrointestinal decontamination

A

Emesis: little evidence of help

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3
Q

Indications for gastric lavage

A 
Within 1 hr of ingestion
Ingested substance not bound by activated charcoal
No effective antidote
Symptomatic
-Intubate
-Lavage
-Cathartic
Make sure airway is secure before you do this!
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4
Q

CIs for gastric lavage

A

Caustic agents
Glass
Sharp objects

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5
Q

Procedure for gastric lavage

A

Large NG tubes
-28-40 French adults
-16-20 French for children
Left Lateral decubitus position
Intubate/secure airway if needed
200-300 mL saline injected then aspirated
First 100 mL sent for toxicology evaluation
LUQ massage to help with breaking up material
Continue until fluid is clear and at least 2 L used

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6
Q

Indications for activated charcoal

A

Presents 1-2 hrs after ingestion

Ingestion of large amount that will bind to charcoal

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7
Q

CIs for activated charcoal

A 
Oral antidote is available
Poor absorption (iron, lithium, heavy metals, alcohols)
> 2 hrs since ingestion
EGD planned/needed
1g/kg is dose with 30 gm max
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8
Q

Polyethylene glycol (PEG) dose

A

1-2 L/hr via NG/OG tube

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9
Q

Indications for polyethylene glycol

A

Removal of drug packets (body stuffers)
Large ingestion of sustained-release drug
Potential toxic ingestion that can’t be treat with activated charcoal (lithium, lead, iron)

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10
Q

CIs for polyethylene glycol

A

Infants
Pts receiving oral antidotes
Dynamic ileus, severe diarrhea, obstruction
Abdominal trauma/recent abdominal surgery

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11
Q

What can be done to enhance elimination?

A 
Multiple-dose activated charcoal (MDAC)
-Repeat dose every 2-4 hrs
-Disrupts the enterohepatic circulation
Urinary alkalinizations
Hemodialysis
-Alkaline diuresis: ionizes weak acids preventing renal reabsorption
--Barbiturates, salicylates, lithium
--1-2 amps NaHCO3 followed by gtt
-Dialysis
--Ethylene glycol, methanol, Paraquat
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12
Q

Presentation of benzodiazepines

A 
Mild-moderate intoxication, based on what they took, how often they take it. 
Lethargy
Slurred speech
Drowsiness
Ataxia
Nystagmus
Coma
Severe intoxication: coma, resp depression
Hypotension
IV overdose has 2% mortality rate
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13
Q

Dx of benzodiazepine toxicity

A 
UDs
Except Klonopin (gas chromatography)
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14
Q

Tx of benzodiazepine toxicity

A

Supportive (airway, BP support)
Flumazenil, GI decontamination efforts
-Don’t use Flumazenil if pt on chronic Benzos. Can cause withdrawal.
Activated charcoal if <1 hr and no significant CNS depression

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15
Q

Examples of sympathomimetics

A 
Ritalin
Adderall
Ephedrine
Cocaine
Methamphetamines
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16
Q

Mechanism of sympathomimetics

A

Increased release of epi, NE from alpha, beta adrenergic receptors, decreased enzymatic breakdown/reuptake

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17
Q

Clinical presentation of sympathomimetic toxicity

A 
Toxidrome:
Agitation
Tachycardia
HTN
Large pupils
Diaphoretic
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18
Q

Dx of sympathomimetic toxicity

A

Clinical presentation (hx and PE)
ECG (establish rhythm and r/o ischemia)
UDS

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19
Q

Tx of sympathomimetic toxicity

A

Supportive care (active/passive cooling measures), IV hydration
Benzodiazepines: for sedation, hyperthermia, muscular rigidity
Sodium bicarb: for wide complex dysrhythmias
Avoid BBs
-Unopposed alpha receptors, will make BP worse

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20
Q

Mechanism of phencyclidine (PCP)

A

Sigma receptor stimulation leads to dysphoria

Antagonism of glutamate activity at NMDA receptor leads to sedation

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21
Q

Clinical presentation of PCP toxicity

A

Distortion of time, space and somatic sensation are hallmark signs
Delusions, hostility, bizarre/violent behavior

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22
Q

Dx of PCP toxicity

A 
Hypoglycemia
Elevated creatinine kinase
AST
ALT
UDS sometimes
-Depends on facility on whether or not it gets tested
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23
Q

Tx of PCP toxicity

A

Reassurance/calming pt
Benzodiazepines
Comatose: intubate

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24
Q

Mechanism of acetaminophen, including how an overdose occurs

A

Metabolized in liver
90% conjugated with glucuronide or sulfate to nontoxic metabolites.
5% oxidized by CYP-450 to NAPQI
Glucuronide can bind to NAPQI forming nontoxic metabolite but in overdoses the stores of glucuronide become depleted
The free NAPQI binds to cellular proteins causing hepatic injury

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25
Q

Phase 1 of acetaminophen toxicity

A

12-24 hrs
N/V
Anorexia
Diaphoresis and pallor

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26
Q

Phase 2 of acetaminophen toxicity

A

Complete return to nl well-being
24 hrs-4 days
Increase in AST, ALT, INR and other liver enzymes
RUQ pain

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27
Q

Phase 3 of acetaminophen toxicity

A 
3-5 days
Symtomatic from hepatic injury
Anorexia
Nausea
Malaise
Abd pain
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28
Q

Phase 4 of acetaminophen toxicity

A

Recovery 5 days- 2 weeks
Regeneration of liver
AST/ALT return to baseline

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29
Q

What tool should be used whether to give an antidote for acetaminophen toxicity?

A

Rumack Matthew nomogram

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30
Q

Activated charcoal and acetaminophen

A

Avidly binds to charcoal

Even up to 8 hrs has shown some benefit

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31
Q

Tx for acetaminophen toxicity

A

N-acetylcysteine
140 mg/kg loading dose
70 mg/kg q4h x 17 doses

32
Q

Special considerations for acetaminophen toxicity

A

Emesis after N-acetylcysteine: Zofran
Pregnancy: consult toxicologist
Chronic EtOH: Treat below nomogram line
Child: use nomogram

33
Q

TCAs

A

Associated with life-threatening CNS and cardiovascular toxicity
Chronic pain
Migraine prophylaxis
Enuresis

34
Q

SSRIs

A

More commonly used

Less toxicity

35
Q

MAOIs

A

Uncommon

36
Q

Clinical presentation of TCA toxicity

A 
Anticholinergic:
Confusion
Anxiety
Delirium
Hallucinations
Hyperactive DTRs
Seizures/coma
Time from ingestion to seizure can be very short
QRS duration >0.10 sec has poor outcome- need EKG
37
Q

Sodium channel blockade in TCAs

A

Causes hypotension with QRS widening >100 msec

38
Q

ECG findings in TCA toxicity

A

Right axis deviation
PR, QRS, QT intervals become prolonged
-QRS >160 msec associated with increased risk wide complex dysrhythmia

39
Q

Tx of TCA toxicity

A

Aggressive
Fluids, GI contamination (lavage if <2 hrs)
Alkalinization pH 7.45-7.55
-RAD, QRS >100 msec, dysrhythmia
Symptomatic bradycardia
-Alkalinization, isoproterenol, pacemaker
-NO atropine
-VTach
–Alkalinization, Lidocaine
Hypotension
-Alkalinization, IV fluids, vasopressors (levophed)

40
Q

Alcohols

A 
Ethanol
-MC poison seen in the ED
Methanol
Ethylene glycol
Isopropyl alcohol
41
Q

Clinical presentation and dx of ethanol toxicity

A

CNS depressant, ataxia, dysarthria, visual impairment, nystagmus
Hx and PE
Serum levels available in ED

42
Q

Tx of ethanol toxicity

A 
ABCs
Other injuries
Thiamine, glucose
Fluids?
Time!
43
Q

Methanol

A

Pain thinner, wood alcohol, windshield wiper fluid
-Accidental ingestion and suicide
Metabolized by ADH to formic acid
-FA accumulation causes anion gap metabolic acidosis, retinal toxicity

44
Q

Clinical presentation of methanol toxicity

A

Similar to ethanol (HA, intoxication, CNS depression)
More pronounced drowsiness
Visual changes: looking through a snow field
-Progresses to blindness

45
Q

Dx of methanol toxicity

A

Anion gap metabolic acidosis with high osmolar gap

46
Q

Tx of methanol toxicity

A

Antidote: Fomepizole or ethanol
-Blocks ADH preventing formic acid production
Folate: improves metabolism of formic acid
Urinary alkalinization: improve renal clearance of FA
Consider hemodialysis with severe acidosis, visual changes

47
Q

Ethylene glycol

A 
Antifreeze
-Colorless, odorless, sweet taste
Metabolized to oxalic acid by ADH
Oxalic acid accumulation causes anion gap metabolic acidosis and direct renal toxicity
100 mL can be fatal
48
Q

Ethylene glycol toxicity dx

A

Anion gap metabolic acidosis with osmolar gap and acute renal failure
Calcium oxalate crystals in UA

49
Q

Clinical presentation of ethylene glycol toxicity

A 
N/V
Ataxia
Nystagmus then to:
Tachypnea and cyanosis, pulmonary edema
Then to: renal failure
50
Q

Tx of ethylene glycol toxicity

A

Antidote: Fomepizole or ethanol
-Complete for ADH and prevent formic acid production
Thiamine and Pyridoxine (Vit B6)
-May help convert oxalic acid to nontoxic metabolites

51
Q

Isopropyl alcohol

A

Rubbing alcohol

Metabolized directly to acetone by ADH

52
Q

Clinical presentation of isopropyl alcohol toxicity

A

CNS depression and severe hemorrhagic gastritis
Hypotension, hypothermia
Death by respiratory arrest

53
Q

Dx of isopropyl alcohol toxicity

A

Serum measurements
Suspect in an intoxicated pt with low/neg EtOH levels
Osmolar gap but no anion gap metabolic acidosis

54
Q

Tx of isopropyl alcohol toxicity

A

Airway/ventilatory support

Fluid resuscitation, vasopressors

55
Q

Clinical presentation of iron toxicity

A

5 phases

1: Abd pain, N/V, gastritis, bloody diarrhea (0-6 hrs)
2: Latent phase (6-24 hrs)
3: Systemic toxicity:
- Metabolic acidosis (lactate), hepatic/renal necrosis and failure
4: Fulminant hepatic failure (2-5 days)
5: Delayed sequelae

56
Q

Dx of iron toxicity

A

Radiographic imaging
-Not always seen
Iron/TIBC not useful due to time (4 hrs)
ABG for acidosis

57
Q

Tx of iron toxicity

A

Admit
Fluids
Deferoxamine- antidote
No GI sx within the first 6 hrs means NO toxicity!
Whole bowel irrigation if seen on abd X-ray
Activated charcoal will not help. Does not bind.

58
Q

Lead toxicity

A

Usually pediatric cases from chronic exposure, not acute ingestion
Think paint chips from old homes

59
Q

Clinical presentation of lead toxicity

A

N/V
Abd pain
Neuropathies
Stupor

60
Q

Dx of lead toxicity

A

Anemia
Red cell stippling on smear
Densities on long bone radiographs

61
Q

Tx of lead toxicity

A

Remove pt from source
Dimercaprol
Calcium disodium edetate (EDTA)
Indication for chelation tx: lead level >70 micrograms/dL or presence of sx

62
Q

Sx/exam of opiate toxicity

A 
CNS depression
Resp depression
Pinpoint pupil
Bradycardia
Hypotension
Hypothermia
63
Q

Dx of opiate toxicity

A

Clinical
Hx and PE
UDS

64
Q

Tx of opiate toxicity

A

Supportive
Naloxone (Narcan)
-Possible SE of neurogenic pulmonary edema: very difficult to correct

65
Q

Withdrawal sx of opiates

A 
Nausea
Vomiting
Diarrhea
Abd pain
Insomnia
Asthenia
66
Q

Anticholinergics

A 
Antipsychotics
Scopolamine
GI anti-spasmotics: Immodium
Muscle relaxers
Antihistamines
Jimsonweed
Deadly nightshade (Atropa belladonna)
67
Q

Mechanism of anticholinergics

A

Competitive antagonism of acetylcholine at muscarinic and CNS cholinergic receptors

68
Q

Sx/exam of anticholinergic toxicity

A 
Agitation, delirium, hallucinations, coma, sz
Hyperthermia, dry/warm skin
Mydriasis and blurred vision
Tachycardia
Urinary retention
69
Q

Dx of anticholinergic toxicity

A

Clinical dx based on hx and physical
EKG to screen for TCA toxicity
Similar to sympathomimetic

70
Q

Tx of anticholinergic toxicity

A 
Supportive care: cooling
IV fluids
Benzodiazepines for seizures/agitation
Antidote: physostigmine
-Only if tachycardia/agitation are not controlled
71
Q

Examples of cholinergics

A 
Donepezil
Pyridostigmine (MG)
Edrophonium
Organophosphates
Pilocarpine (glaucoma)
72
Q

Mechanism of cholinergics

A

Inhibition of enzyme acetylcholinesterase leading to excess acetylcholine at muscarinic/nicotinic receptors

73
Q

Sx of cholinergic toxicity

A 
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
"Killer bees"
-Bronchospasm
-Bradycardia
-Bronchorrhea
AMS, seizures
74
Q

Dx of cholinergic toxicity

A

Hx and PE
EKG to screen for blocks/dysrhythmias
RBC cholinesterase levels

75
Q

Tx of cholinergic toxicity

A 
Supportive
Atropine (high doses)
-Hemodynamically unstable bradycardia
-Excessive secretions
Benzodiazepines for seizures/agitation
Antidotes:
-Atropin
-Pralidoxime (2-PAM) for organophosphate poisoning

Emergency Med (11 decks)

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