Toxicology Flashcards

1
Q

Basic Principles of Toxocology

A
  1. Keep ingestion on your radar
  2. Obtain a detailed hx
  3. Be familiar with common toxidromes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Lab evals

A

-Glucose
-CBC
-Extended electrolytes
-Lactate
-ABG (carboxyhemoglobin, methemoglobin)
-Acetaminophen and salicylate levels
-Ethanol
-Urine drug screen
-Pregnancy test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ECG

A

-Many toxin cause cardiotoxic affects
-QRS widening
-Tall R-waves
-QTc prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sodium Channel Blockers

A

-TCAs
-Cocaine
-Benadryl
-Flexeril
-Tegretol
-Propafenone
-Flecainide
-Sodium bicarbonate if QRS <120 msec (50-100 mEq bolus, then infusion 150 mEq/Liter D5W at 150 ml/hour
Serum pH 7.45-7.55;
Check pH and K+ q 2 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Agitation Management

A

-Benzodiazepines
-Avoid Haldol
b/c
—impairs heat dissipation
—Prolongs QTc
—worsens anticholinergic toxicity
—lower seizure threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Classic toxidromes

A

-Opioids
-Sedatives/Hypnotics
-Sympathomimetic
-Hallucinogenic
-Serotonin
-Anticholinergic/cholinergic
-Acetaminophen
-Salicylates
-BB/Ca Channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Opioids

A

-Bind to opioid receptors such as Mu, Kappa, Delta
-Ex: morphine, fentanyl, tramadol, methadone, heroin, meperidine, hydrocodone, oxycodone, hydromorphone
-CNS Depression, hypoventilation, miosis, hotn, rhabdomyolysis if found down, noncardiognic pulmonary edema w/ progression of ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Opioid Tx

A

-O2, airway support, naloxone
-Nalmefene is similar to narcan but has longer half life at 10 hours. Naloxone is the preferred choice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Naloxone (Narcan)

A

-Mu receptor antagonist. Pushed opioids out of the receptors and binds them to themselves.
-half life is 1 hours.
-Don’t push all at once, slowly awaken patient
-0.04 to 0.4 mg IV every 2-3 minutes; repeat dose or increase to 2 mg if inadequate
-If no response with 5-10 mg, probably not opioid overdose
-Continuous infusion 0.05 mg/hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Naloxone (Narcan) Precautions

A

-May precipitate acute withdrawal symptoms and seizures
-May lead to pulmonary edema
-CNS depression may return after initial improvement due to short half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sedatives/Hypnotics

A

-Benzos, ethanol, barbiturates, zolpidem
-Cause anesthesia with diminished reflex activity and loss of awareness
-CNS depression
-Hyporeflexia
-Depressed respiratory rate with large quantities
-Hypothermia
-Hotn
-mild bradycardia
-Ataxia
-Pupils normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Sedative & Hypnotics Tx

A

-Supportive, o2 and airway, ETOH monitoring, benzos: Flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Flumazenil

A

-0.2 mg IV, followed by 0.3 mg, 0.5 mg if no effect
-Max 3 mg/hour
-If 5 mg in one hour ineffective, likely to be something other than benzodiazepine
-Half life: 54 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Flumazenil Precautions

A

-Black box warning: increased risk of seizures, especially in patients w/ concurrent sedative-hypnotic withdrawal
-Re-sedation may occur
-May precipitate benzo withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sympathomimetics

A

-Designer drugs, PCP, ecstasy, cocaine, synthetic cathinone, ephedrine, beta-adrenergic agonists, amphetamines, caffeine
-Increase activity of alpha & beta receptors
-Found in the skin, eyes, heart, GI tract, lungs, exocrine glands
-Cause: tachycardia, htn, tachypnea, agitation (at someone or something)
-Diaphoresis, mydriasis, seizures, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sympathomimetics Tx

A

-No antidote
-Keep patient safe
-Tx: Benzodiazepines
0.02 to 0.06 mg/kg IV every 2-6 hours
Patient dependent!
-Sodium bicarbonate infusion for cardiac stabilization
(50-100 mEq bolus, then infusion 150 mEq/Liter D5W at 150 ml/hour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Serotonergics

A

-Serotonergics are agents that modify the effect of serotonin in the body
-Psychedelic stimulants, Dextromethorphan, SSRIs, TCAs, MAOIs, Buspirone, lithium, meperidine, linezolid, ecstasy
-Clinical triad: autonomic instability (HR, temp increase), agitated delirium, neuromuscular agitation (hyperreflexia, clonus)
-Akathisia, tremor, diaphoresis, diarrhea, rhabdomyolysis, pupils normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Serotonergics Tx

A

-Supportive care, d/c all serotonergic agents (tramadol, fentanyl). IV fluids, avoid restraints, active cooling
-Benzos, propofol +/- paralytics, Cyproheptadine vs Chlorpromazine, Precedex
—-Benzos are the cornerstone of tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cyproheptadine

A

-Serotonergic tx
-Nonspecific serotonin antagonist.
-histamine-1 receptor antagonist with nonspecific 5-HT1A and 5-HT2A antagonistic properties.
-Initial dose of 12 mg, followed by 2 mg every 2 hours until desired clinical response.
-Needs further research
-Only oral form

20
Q

Chlorpromazine

A

-Serotonergic tx
-Not well studied. Not recommended.
-Antipsychotic agents with 5-HT2A antagonist activity.
-Exact mechanism of action is unknown, though is thought to have mild anti-serotonin activity.

21
Q

Dexmedetomidine hydrochloride (Precedex)

A

-Alpha-2 adrenergic agonist with sedative characteristics.
-Loading dose 1 mcg/kg over 10 minutes
-Maintenance for < 24 hours 0.15 to 1.5 mcg/kg/hr
-Maintenance for > 24 hours 0.2 to 0.7 mcg/kg/hr
-Monitor for bradycardia and hypotension

22
Q

Anticholinergics

A

-Meds association w/ parasympathetic nervous system
-Innervates the eyes, heart, respiratory system, skin, GI/GU, sweat glands
-Diphenhydramine, TCAs, Antipsychotics, jimson weed, angels trumpet, antiparkinsonian, atropine, nightshade (belladonna)
-Tachycardia, hyperthermia, variable BP, Tachypnea, mydriasis, redirectable delirium.

23
Q

Anticholinergic Tx

A

-Supportive cares
-Monitor for seizures, treat with Benzodiazepines
-Cardiac monitoring for prolonged QRS, QTc
-Avoid haloperidol (seizure, dysrhythmias, qtc prolongation)
-Physostigmine: contraindicated in TCAs

24
Q

Physostigmine

A

-Anticholinergic tx
-Crosses the BBB to inhibit cholinesterase and makes more acetylcholine available
-2 mg IV (slowly, 1 mg/min)
-May repeat dose for life threatening signs
-Works quickly, half life 4.9 hours
-Monitor for bradycardia and convulsions if administered too quickly
-Excessive cholinergic effects may occur

25
Cholinergics
-Activates the muscarinic acetylcholine receptors -Nerve gas, insecticides, physostigmine, donepezil, muscarinic mushrooms -Defecation, Urination Miosis, Bradycardia -Bronchospasm, emesis, lacrimation, secretions, seizures.
26
Cholinergic Tx
-Decontamination, d/c agent, supportive therapy, IV fluids, atropine (even w/ tachycardia), glycopyrolate -Atropine -Pralidoxime
27
Atropine for Cholinergic tx
-2 to 3 mg IV/IM/SQ; may repeat in 20 to 30 minutes -Titrate based on HR, PR interval, symptoms -In intubated ICU patients: initial dose 20 mg IV in combination with pralidoxime 2 g IV loading dose
28
Acetaminophen Metabolism
-rapidly absorbed from the stomach and small intestine. -Serum levels peak in 1-2 hours, level 5-20 ug/ml, plasma peak in 4 hours. -Elimination half-life is 2 hours, unless hepatic dysfunction, then up to 17 hrs. -Excess acetaminophen is metabolized via the CYP enzymes to the hepatotoxic reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI).
29
Risk factors for acetaminophen toxicity
-underlying hepatic or renal disease -older age, restricted diet, compromised immune system nutritional status -Ethanol ingestion, Tobacco smoking Isoniazid (INH), Rifampin Phenytoin, Phenobarbital Barbiturates, Carbamazepine, Trimethoprim-sulfamethoxazole (TMP-SMZ), Zidovudine
30
Phase 1: First 24 hours of acetaminophen toxicity
-Asymptomatic Anorexia, nausea, vomiting, malaise
31
Phase 2: 18-72 hrs after ingestion (if untreated) acetaminophen toxicity
-RUQ pain, anorexia, nausea, vomiting Tachycardia and hypotension
32
Phase 3: 72-96 hrs (if untreated) acetaminophen toxicity "hepatic phase"
Nausea, vomiting, abdominal pain Hepatic necrosis/synthetic dysfunction --- Jaundice, encephalopathy, coagulopathy, hypoglycemia, LFTs extremely elevated and peak (AST>10000), acute renal failure possible
33
Phase 4: 4 days to 3 days post-ingestion acetaminophen toxicity
-Either death, complete recovery or transplant -May take several months for complete hepatic recovery
34
Acetaminophen Tx
-Charcoal (within 4 hours of ingestion) -N-acetylcystine IV or PO IV Loading dose (41-99 kg): 150 mg/kg IV over one hour IV Maintenance: 50 mg/kg over 4 hours; 100 mg/kg over 16 hours Oral: 140 mg/kg PO initial dose; then 70 mg/kg every 4 hours over 16 hours -WI vs MN
35
Discontinuation of N-acetylcystine
INR Acetaminophen undetectable Transaminases decreasing
36
Salicylate toxicity
-Medical emergency -Early/mild symptoms: Tinnitus, vertigo, nausea, vomiting, diarrhea -Late/severe symptoms: Encephalopathy (from agitation to lethargy), hyperpyrexia, noncardiac pulmonary edema -Symptoms present in 1-2 hrs after ingestion (enteric coated)
37
Salicylate tx
-Admit for ingestions of 150 mg/kg or greater OR TOXICITY -Decontamination -intubation -Volume status -Alkalinization of urine -Supplemental glucose
38
Ca channel blockers/Beta blockers
-bradycardia, hotn, dysrhytmias, shock -Propranolol is the most toxic beta-blocker and the most frequently used in suicide attempts worldwide. -Historically treated with IV fluids, inotropes, pacing, glucagon, lipids -Evidence suggests that high dose insulin therapy may be beneficial in refractory cardiogenic shock secondary to CCB and BB overdose
39
MOA Ca Channel blocker toxicity
-Disrupt fatty acid metabolism and create relative insulin resistance in the myocardium
40
MOA of BB toxicity
Interfere with myocyte metabolism, and inhibits pancreatic insulin release.
41
Goals of toxicology insulin dosing
-Maintain CO & Perfusion -Titrate off vasopressors -Glucose 150-250 mg/dL -K 2.5-3 -Ical 5-6 mg/dL -Give Ca -Bolus dextrose, followed by infusion of D50 at 150 ml/hr -Regular insulin IV, bolus dose 1 unit/kg-Max dose (10 unites/kg/hr)
42
Anion Gap
Na – (Cl + HCO3) -Normal 4-12 mmol/L -Total cations: Sodium -Total anions: chloride, bicarbonate -Methanol, metformin -Ethylene glycol -Toluene -Alcoholic ketoacidosis -Lactic acidosis -Aminoglycosides -Cyanide, carbon monoxide -Isoniazid, iron -Diabetic ketoacidosis -Generalized seizure-producing toxins -Aspirin -Paraldehyde, phenformin
43
Anion Gap Mnemonics
Methanol Uremia Diabetic ketoacidosis Paraldehyde Isoniazid/Iron Lactate Ethylene glycol Salicylate
44
Osmolar Gap
-Take with anion gap -detects unmeasured compounds in the serum -Normal value < 10 -High osmolar gap can indicate the presence of an extra solute, such as methanol or ethylene glycol
45
Osmolar Gap Mnemonic
-Methanol -Ethylene glycol -Diuretics (osmotic diuretics like mannitol) -Isopropyl alcohol -Ethanol