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PCOL Cumulative Final > Final Exam Toxicology > Flashcards

Final Exam Toxicology Flashcards

1
Q

Cholinergic Toxidrome

A

SLUDGE

Salivation

Lacrimation

Urination

Defecation

Gastrointestinal Symptoms

Emesis

Triple B’s/Killer B’s

Bronchorrhea

Bradycardia

Bronchospasm

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2
Q

Anticholinergic Toxidrome

A
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3
Q

Sympathetic Toxidrome

A

Agitation

Anxiety

Bronchodilation

HTN

Mydriasis

Tachycardia

Urinary Retention

Seizures

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4
Q

Toxidrome Comparison

A
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5
Q

Treatment Strategies

A

Prevent absorption

Enhance elimination

Block effects

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6
Q

GI Decontamination: Activated Charcoal

A
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7
Q

Other Methods of GI Decon

A

Emesis

Not recommended

Gastric Lavage

Scare evidence

Use within 30-60 minutes of ingestion

Cathartics

No indication for routine use

Whole Bowel Irrigation

Large amount of osmotically balanced polyethylene glycol electrolyte lavage solution

Ingestion of toxic amount of drug that is not adsorbed to activated charcoal, ER preparations, or Body packers

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8
Q

When is Activated Charcoal NOT Useful

A

Caustic/corrosive solution

Heavy metals (iron/lead/mercury)

Alcohols

Rapidly absorbed substances

Cyanide

Organophosphates

Aliphatic hydrocarbons

Lithium

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9
Q

Hemodialysis

A
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10
Q

Urinary Alkalization

A
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11
Q

Opioids

A

Causative agents: Buprenorphine, Codeine, Fentanyl, Heroin, Hydrocodone, Hydromorphone, Meperidine, Methadone, Morphine, Oxycodone, Oxymorphone, Tapentadol, Tramadol

Mechanism of toxicity: Increased stimulation of opioid receptors

Receptor and Clinical effects

u – Analgesia, sedation, euphoria, respiratory, depression, GI dysmotility, bradycardia, pruritis, physical dependence

k – Analgesia, miosis

g – Analgesia

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12
Q

Opioid Overdose: Clin Presentation

A

Sedation

Respiratory distress

Bradycardia

Hypotension

Miosis

Emesis

Constipation

Seizures (meperidine, tramadol)

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13
Q

Overdose Treatment: Naloxone (Narcan)

A

MOA: Competitively inhibits binding of opioids to opioid receptors

Goals of therapy: Reinstitution of spontaneous ventilation

Use lower practical dose; escalate rapidly as clinically indicated

IV: 0.4-2 mg as initial dose

Repeat dose at 2-3 minute intervals

Consider other causes of toxicity if no response after 10mg of naloxone

Adverse Reaction: Withdrawal

Pharmacokinetics: T1/2 = 30-90 minutes

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14
Q

Benzodiazepines and Barbiturates

A
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15
Q

Benzodiazepines and Barbiturates: Clin Presentation

A
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16
Q

Benzodiazepines and Barbiturates: Management and Monitoring

A

Supportive Care

Maintain airway

Hemodynamic support

Minimum 24h monitoring period for overdoses on long-acting hypnotics or drugs with significant enterohepatic recirculation

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17
Q

Benzodiazapine Antidote: Flumazenil

A

MOA: Competitive benzodiazepine antagonist

Rapidly reverses sedative effect of benzodiazepines and Zolpidem

Dose:

0.2mg over 30 seconds

Repeat doses: 0.2 mg over 30 seconds repeated at 1-min intervals

Maximum Cumulative Dose: 3mg (usual total dose 1-3 mg)

Caution: May precipitate benzo withdrawal

Boxed Warning: Seizures

Caution in multi-substance overdoses

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18
Q

Beta Blocker & Calcium Channel Blocker Toxicity

A

Beta Blockers

B1 selective: Acebutolol, Atenolol, Betaxolol, Bisoprolol, Esmolol, Metoprolol, Nebivolol

Mixed: Carvedilol, Labetalol, Propranolol

Calcium Channel Blockers

Dihydropyridine: Amlodipine, Nicardipine, Nifedipine, Nimodipine

Non-dihydropyridine: Verapamil, Diltiazem

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19
Q

Beta Blocker & Calcium Channel Blocker Toxicity Clinical Presentation

A

Bradycardia

Hypotension

CCB-Specific

Vasodilatory shock

Hyperglycemia

Dihydropyridines: Reflex tachycardia in mild – moderate overdose

BB-Specific

Propranolol: Hypoglycemia, seizures, coma, and dysrhythmias

Prolonged QRS and QT intervals

Rare: Prolonged PR interval or high-grade AV block

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20
Q

Beta Blocker & Calcium Channel Blocker Mechanism of Toxicity

A
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21
Q

BB/CCB Supportive care

A

Early airway and respiratory support

Early GI decon

Activated charcoal (single dose) for all IR ingestions if within 4 hours

Whole Bowel irrigation (polyethylene glycol electrolyte mixture) for SR preparations if early and Asymptomatic

Manage Shock

Isotonic IV fluids: Limit 1-2 L to avoid fluid overload and pulmonary edema

Symptomatic bradycardia

Cutaneous and transvenous pacing

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22
Q

BB/CCB Pharmacotherapy PT 1 (Atropine/Calcium)

A
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23
Q

BB/CCB Pharmacotherapy PT 2 (Glucagon)

A
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24
Q

BB/CCB Pharmacotherapy PT 3 (Catecholamines)

A
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25
Q

BB/CCB Pharmacotherapy PT 4 (High-dose insulin euglycemia therapy (HIET))

A
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26
Q

Specific Pharmacotherapy

A
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27
Q

Monitoring

A

Observe in the ICU until bradycardia, hypotension, EKG abnormalities, and/or CNS Toxicity resolve

Beta Blockers

Toxicity from regular release beta blockers poisoning typically occurs within the first 6 hours

Sotalol: Delayed ventricular dsyrhythmias up to 9 hours post-ingestion

Observe PTs who ingest ER preparations for at least 24 Hours

Calcium Channel Blockers

If IR preparation ingestion, ensure that serial EKGs over 6-8 Hours have remained unchanged

Observe PTs who ingest ER products for at least 24 Hours, even if asymptomatic

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28
Q

Digoxin

A

Cardioactive steroid used for management of supraventricular arrhythmias and heart failure

MOA:

Inhibition of the Na/K/ATPase pump in myocardial cells

Increased intracellular Ca via Na/Ca exchange pump

Increased myocardial contractility

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29
Q

Digoxin Toxicity Diagnosis

A

Therapeutic range 0.4-2 ng/mL

Suggestion to lower upper limit 1ng/mL

Clinical presentation

Symptoms

Electrolyte abnormalities

EKG findings

Timing of Symptom onset

Acute vs chronic toxicity

30
Q

Digoxin Toxicity: Clin Presentation

A
31
Q

The Digitalis Effect

A
32
Q

Digoxin Antidote: DigiFab

A

Digifab: Digoxin-specofoc antibody fragments

Binds with digoxin to decrease serum digoxin concentration (SDC)

Increased Renal clearance of Bound Digoxin

Dosing

Emperic dosing

  • Acute: 10-20 vials
  • Chonic: 3-6 Vials

Known Amount

-Calculate Total Body Load:

–Capsules: amount (mg) digoxin capsules ingested

–Tablets 0.8 x amount (mg) digoxin tablets ingested

-Calculate number of vials needed

–Total body load (mg)/0.5

33
Q

DigiFab indications

A
34
Q

Acetaminophen Overdose: Clinical Presentation

A
35
Q

APAP Toxic Doses

A

Acute Toxicity

Single Ingestion of 150 mg/kg

Chronic Toxicity

Less well defined

Evaluate in PTs taking more than 200 mg/kg/d (or 10 g/d) in 24H

Evaluate in PTs taking more than 150 mg/kg/d (or 6 g/d) in 48H

36
Q

Factors Affecting APAP Toxicity

A

APAP dose

Pattern of use

Acute vs Chronic alcohol ingestion

Concomitant Medication ingestion

Age

Nutritional status

Presence of Chronic liver disease

37
Q

APAP Toxicity Supportive Care

A

GI Decon with Activated Charcoal

If within 4 hours of acute APAP ingestion

May be given after 4 hours if extended-release APAP ingestion of drugs that delay gastric emptying time

Liver Transplant

Lifesaving procedure when APAP ingestion has progressed to irreversible liver failure

Qualifying factors: Poor projected outcome and high risk of mortality based on MELD, Kings Criteria, and Apache II scores

38
Q

Pharmacotherapy: N-Acetylcysteine (NAC)

A

Cysteine prodrug and hepatic GCH precursor

Replenishes and maintains hepatic GCH stores by providing Cysteine, which detoxifies reactive metabolites of APAP

May reduce NAPQI back to APAP by enhancing Sulfonation pathway

May reduce mortality from 5% to 0.7%

39
Q

Utility of Rumack-Matthew Nomogram

A
40
Q

Unknown Time of Ingestion: To Treat or not to Treat

A

If Normal APAP and Normal AST/ALT do not treat, otherwise TREAT

41
Q

Treatment Duration

A

Decision to discontinue NAC after extending treatment beyond standard protocol length is PT specific and should be continued if:

Evidence of hepatic injury

  • AST significantly above normal
  • PT/INR> twice normal
  • Encephalopathy

APAP metabolism is incomplete (APAP detectable)

Continue treatment with NAC until evidence of hepatic injury resolves and APAP is undetectable

42
Q

Organophosphates

A

Agents: Malathion, Parathion, methyl parathion, diazinon

MOA/Mechanism of Toxicity: Increased concentration of acetylcholine (ACh) at muscarinic and nicotinic cholinergic synapses-> cholinergic excess

43
Q

Organophosphate Clin Presentation

A
44
Q

Management of Organophosphate Tox

A

Atropine MOA: Competitive antagonist of AcH at muscarinic receptors; reverses excessive secretions, miosis, bronchospasm, vomiting, diarrhea, diaphoresis, and urinary incontinence

Pralidoxime (2-PAM) MOA: Enhances regen of AChE to lower ACh concentrations and improve muscarinic and nicotinic effects

45
Q

Serotonin Overview

A

Serotonin (5-HT): Monoamine neurotransmitter synthesized from tryptophan

5-HT1A and 5-HT2A most commonly implicated in serotonin syndrome

Found in the CNS, platelets, and GI tract

CNS: regulates appetite, memory, mood, and sexual activity

Peripherally: Assists in regulating clotting, peristalsis, and vascular tone

L-Tryptophan -> 5 Hydroxytryptamine (Serotonin)

46
Q

Causative Agents

A

Increased Serotonin Production – L-Tryprophan

Inhibition of serotonin reuptake – Chlorpheniramine, cyclobenzaprine, dextromethorphan, meperidine, methadone, pentazocine, SSRIs, St. John’s wort, Tramadol, trazodone, TCAs

Inhibition of serotonin metabolism by MAO – Linezolid, methylene blue, phenelzine, selegiline

Increased serotonin release – Dextromethorphan, meperidine, methadone, MDMA, mirtazapine, Fentanyl, cocaine, amphetamines

Stimulation of Serotonin receptors – Buspirone, lithium, LSD, Meperidine, metoclopramide, triptans

47
Q

Diagnosis

A

Diagnosis of exclusion – no confirmatory test

Assess exposure to serotonergic drugs in the last 5 weeks

Monitor signs/Symptoms of serotonin syndrome

Obtain Labs tox screen

48
Q

SS Clin Presentation

A
49
Q

Differential Diagnosis: SS vs Neuroleptic Malignant Syndrome (NMS)

A
50
Q

Supportive Care of SS

A

Discontinue offending agent

Administer IV fluids

Control hemodynamic instability

Benzo for agitation

Implement standard cooling measures for hyperthermia

Severe toxicity may warrant sedation, paralysis &/or intubation

51
Q

Pharmacotherapy for SS

A
52
Q

Monitoring

A

Typically resolves within 24H of cessation of serotonergic drug

Admit and monitor 12-24 Hrs

Concern for delayed cardiotoxicity

53
Q

TCA

A

Mechanism of Toxicity

Inhibition of Serotonin and norepinephrine reuptake at nerve terminals

Direct a adrenergic block

Membrane stabilizing effect

Anticholinergic action

54
Q

TCA Clin Presentation

A
55
Q

TCA Management

A
56
Q

TCA Monitor

A
57
Q

Stimulant Toxicity

A

Causative Agents

Amphetamines/Dextroamphetamines/Methamphetamines

Methylenedioxymethamphetamine (MDMA/Ecstasy)

Synthetic Cathinones (bath salts)

Methylphenidate

Cocaine

58
Q

Stimulant OD Management/Supportive care

A
59
Q

Toxic Alcohols

A
60
Q

Clin Presentation of Methanol

A
61
Q

Clin Presentation of Ethylene Glycol

A
62
Q

Clin Presentation of Isopropanol

A
63
Q

Mechanism of Alcohol Toxicity

A
64
Q

Supportive care for Alcoholic Toxicity

A
65
Q

The Role of Vitamins in Alcohol Toxicity

A
66
Q

Treatment indications of Alcohol Toxicity

A
67
Q

Alcohol Antidotes: Ethanol and Fomepizole

A

Not as helpful with isopropanol

68
Q

Pharmacotherapy: Fomepizole

A
69
Q

Pharmacotherapy: Ethanol

A
70
Q

Co-Ingestion of Ethanol

A

PCOL Cumulative Final (14 decks)

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