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Emergency Med > Toxicology > Flashcards

Toxicology Flashcards

(75 cards)

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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
Phase 1 of acetaminophen toxicity
12-24 hrs N/V Anorexia Diaphoresis and pallor
26
Phase 2 of acetaminophen toxicity
Complete return to nl well-being 24 hrs-4 days Increase in AST, ALT, INR and other liver enzymes RUQ pain
27
Phase 3 of acetaminophen toxicity
``` 3-5 days Symtomatic from hepatic injury Anorexia Nausea Malaise Abd pain ```
28
Phase 4 of acetaminophen toxicity
Recovery 5 days- 2 weeks Regeneration of liver AST/ALT return to baseline
29
What tool should be used whether to give an antidote for acetaminophen toxicity?
Rumack Matthew nomogram
30
Activated charcoal and acetaminophen
Avidly binds to charcoal | Even up to 8 hrs has shown some benefit
31
Tx for acetaminophen toxicity
N-acetylcysteine 140 mg/kg loading dose 70 mg/kg q4h x 17 doses
32
Special considerations for acetaminophen toxicity
Emesis after N-acetylcysteine: Zofran Pregnancy: consult toxicologist Chronic EtOH: Treat below nomogram line Child: use nomogram
33
TCAs
Associated with life-threatening CNS and cardiovascular toxicity Chronic pain Migraine prophylaxis Enuresis
34
SSRIs
More commonly used | Less toxicity
35
MAOIs
Uncommon
36
Clinical presentation of TCA toxicity
``` 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
Sodium channel blockade in TCAs
Causes hypotension with QRS widening >100 msec
38
ECG findings in TCA toxicity
Right axis deviation PR, QRS, QT intervals become prolonged -QRS >160 msec associated with increased risk wide complex dysrhythmia
39
Tx of TCA toxicity
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
Alcohols
``` Ethanol -MC poison seen in the ED Methanol Ethylene glycol Isopropyl alcohol ```
41
Clinical presentation and dx of ethanol toxicity
CNS depressant, ataxia, dysarthria, visual impairment, nystagmus Hx and PE Serum levels available in ED
42
Tx of ethanol toxicity
``` ABCs Other injuries Thiamine, glucose Fluids? Time! ```
43
Methanol
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
Clinical presentation of methanol toxicity
Similar to ethanol (HA, intoxication, CNS depression) More pronounced drowsiness Visual changes: looking through a snow field -Progresses to blindness
45
Dx of methanol toxicity
Anion gap metabolic acidosis with high osmolar gap
46
Tx of methanol toxicity
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
Ethylene glycol
``` 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
Ethylene glycol toxicity dx
Anion gap metabolic acidosis with osmolar gap and acute renal failure Calcium oxalate crystals in UA
49
Clinical presentation of ethylene glycol toxicity
``` N/V Ataxia Nystagmus then to: Tachypnea and cyanosis, pulmonary edema Then to: renal failure ```
50
Tx of ethylene glycol toxicity
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
Isopropyl alcohol
Rubbing alcohol | Metabolized directly to acetone by ADH
52
Clinical presentation of isopropyl alcohol toxicity
CNS depression and severe hemorrhagic gastritis Hypotension, hypothermia Death by respiratory arrest
53
Dx of isopropyl alcohol toxicity
Serum measurements Suspect in an intoxicated pt with low/neg EtOH levels Osmolar gap but no anion gap metabolic acidosis
54
Tx of isopropyl alcohol toxicity
Airway/ventilatory support | Fluid resuscitation, vasopressors
55
Clinical presentation of iron toxicity
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
Dx of iron toxicity
Radiographic imaging -Not always seen Iron/TIBC not useful due to time (4 hrs) ABG for acidosis
57
Tx of iron toxicity
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
Lead toxicity
Usually pediatric cases from chronic exposure, not acute ingestion Think paint chips from old homes
59
Clinical presentation of lead toxicity
N/V Abd pain Neuropathies Stupor
60
Dx of lead toxicity
Anemia Red cell stippling on smear Densities on long bone radiographs
61
Tx of lead toxicity
Remove pt from source Dimercaprol Calcium disodium edetate (EDTA) Indication for chelation tx: lead level >70 micrograms/dL or presence of sx
62
Sx/exam of opiate toxicity
``` CNS depression Resp depression Pinpoint pupil Bradycardia Hypotension Hypothermia ```
63
Dx of opiate toxicity
Clinical Hx and PE UDS
64
Tx of opiate toxicity
Supportive Naloxone (Narcan) -Possible SE of neurogenic pulmonary edema: very difficult to correct
65
Withdrawal sx of opiates
``` Nausea Vomiting Diarrhea Abd pain Insomnia Asthenia ```
66
Anticholinergics
``` Antipsychotics Scopolamine GI anti-spasmotics: Immodium Muscle relaxers Antihistamines Jimsonweed Deadly nightshade (Atropa belladonna) ```
67
Mechanism of anticholinergics
Competitive antagonism of acetylcholine at muscarinic and CNS cholinergic receptors
68
Sx/exam of anticholinergic toxicity
``` Agitation, delirium, hallucinations, coma, sz Hyperthermia, dry/warm skin Mydriasis and blurred vision Tachycardia Urinary retention ```
69
Dx of anticholinergic toxicity
Clinical dx based on hx and physical EKG to screen for TCA toxicity Similar to sympathomimetic
70
Tx of anticholinergic toxicity
``` Supportive care: cooling IV fluids Benzodiazepines for seizures/agitation Antidote: physostigmine -Only if tachycardia/agitation are not controlled ```
71
Examples of cholinergics
``` Donepezil Pyridostigmine (MG) Edrophonium Organophosphates Pilocarpine (glaucoma) ```
72
Mechanism of cholinergics
Inhibition of enzyme acetylcholinesterase leading to excess acetylcholine at muscarinic/nicotinic receptors
73
Sx of cholinergic toxicity
``` Salivation Lacrimation Urination Defecation GI upset Emesis "Killer bees" -Bronchospasm -Bradycardia -Bronchorrhea AMS, seizures ```
74
Dx of cholinergic toxicity
Hx and PE EKG to screen for blocks/dysrhythmias RBC cholinesterase levels
75
Tx of cholinergic toxicity
``` 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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