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ITE '23 > Ch. 6 Tox > Flashcards

Ch. 6 Tox Flashcards

1
Q

What are indications for gastric lavage?

A

Ingestion of a substance with high-toxic potential and:
■ Within 1 hour of ingestion.
■ Ingested substance is not bound by AC or has no effective antidote.
■ Potential benefits outweigh risks.

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2
Q

When performing gastric lavage, what is the recommended tube size for adults? children?

A

36F-40F for adults, 22F-28F for children

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3
Q

When performing gastric lavage, how should the patient be positioned?

A

left-lateral decubitus position, with head lowered below level of feet

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4
Q

When performing gastric lavage, what solution is used for lavage?

A

250 mL (10-15 mL/kg in children) aliquots of warm water or saline

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5
Q

What is the end point for gastric lavage?

A

Continue until fluid is clear and a minimum of 2 L has been used

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6
Q

What are common agents that cause anticholinergic toxidrome?

A

antihistamines
Jimsonweed (scopalamine)
Deadly nightshade (atropine)

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7
Q

What are the signs and symptoms of anticholinergic toxidrome?

A

Altered mentation
Dry, flushed skin
Mydriasis
Hyperthermia
Seizures
Tachycardia
Urinary retention

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8
Q

What is the treatment for anticholinergic toxicity?

A

Benzodiazepines
Physostigmine

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9
Q

What agents cause cholinergic toxidrome?

A

Organophosphates
Carbamates
Sarin

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10
Q

What are signs and symptoms of Cholinergic toxicity?

A

Altered mentation
Bradycardia
Bronchospasm
↑ Secretions
Miosis
nausea/vomiting,
defecation
Seizures
Urination

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11
Q

What is the treatment for cholinergic toxicity?

A

Atropine 2-PAM (for
organophosphates)

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12
Q

What agents can cause a sympathomimetic toxidrome?

A

Ephedrine
Ma Huang (Ephedra) (an evergreen shrub)
Cocaine
Amphetamines

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13
Q

What are signs and symptoms of sympathomimetic toxicity?

A

Agitation
Diaphoresis
Hallucinations
HTN
Hyperthermia
Mydriasis
Muscular rigidity
Tachycardia

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14
Q

What is treatment for sympathomimetic toxicity?

A

Benzodiazepines
Sodium bicarbonate (for wide complex dysrhythmias)

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15
Q

What agents cause opioid toxidrome?

A

Morphine
Heroin

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16
Q

What are signs and symptoms of opioid toxicity?

A

CNS depression
Bradycardia
Hypothermia
Miosis
Respiratory depression

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16
Q

What are signs and symptoms of opioid toxicity?

A

CNS depression
Bradycardia
Hypothermia
Miosis
Respiratory depression

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16
Q

What are signs and symptoms of opioid toxicity?

A

CNS depression
Bradycardia
Hypothermia
Miosis
Respiratory depression

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17
Q

What is the treatment for opioid toxicity?

A

Naloxone

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18
Q

How is activated charcoal dosed?

A

AC should be given in a 10:1 ratio (ie, ingestion of 1 g of poison requires 10 g of AC), so larger or repeated doses may be required in cases of massive
overdose.
■ Empiric dosing typically starts with 50-100 g (1 g/kg in children).

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19
Q

For what ingestions is activated charcoal contraindicated?

A

metals (iron, lead, lithium)
alcohols
caustics or hydrocarbons – bc greater danger if AC induced vomiting

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20
Q

What solution and dose is used for Whole Bowel Irrigation (WBI)?

A

Polyethylene glycol (PEG) solution is administered at a rate of 1-2 L/h (usually requires a naso- or orogastric tube)

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21
Q

What is the desired endpoint for whole bowel irrigation?

A

clear rectal effluent or a total irrigation volume of 10 L

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22
Q

When is Whole Bowel Irrigation indicated?

A

Removal of ingested drug packets (eg, body packers) without suspicion of packet rupture, large ingestion of a sustained-release drug, or potentially
toxic ingestion that cannot be treated with AC (eg, metals)

Common indications for WBI: Body packers,
sustained-release formula medications,
and metals.

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23
Q

What are contraindications for whole bowel irrigation?

A

Diminished level of consciousness/unprotected airway reflexes (intubate first),
decreased GI motility,
bowel obstruction,
significant GI hemorrhage,
or persistent emesis

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24
Q

What is Multiple-Dose Activated Charcoal and when is it indicated?

A

repeated doses of AC (every 2-4 hours) to increase poison clearance

Drugs with:
- enterohepatic or enteroenteric circulation,
- sustainedrelease agents, and
- agents that form concretions or bezoars can possibly be treated with MDAC include the following: Carbamazepine, dapsone,
phenobarbital, quinine, and theophylline.

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25
Q

With what ingestions is urinary alkalinization indicated?

A

Aspirin
Methotrexate
Phenobarbital

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26
Q

How is urinary Alkalinization achieved?

A

sodium bicarbonate (NaHCO3) infusion

The most common method uses 150 mEq of NaHCO3 (3 amps) in 1 L D5W, infused at 1.5 to 2 × the normal intravenous (IV) fluid maintenance rate

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27
Q

What is a contraindication to urinary alkalinization?

A

Patients who cannot tolerate excess sodium/water loading (eg, congestive heart failure [CHF], renal failure)

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28
Q

What drug ingestions can commonly cause Bradydysrhythmias (sinus bradycardia, AV block)?

A

b-Blockers
Ca++ channel blockers
Cardiac glycosides
Clonidine
Other antidysrhythmic agents

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29
Q

What drug ingestions can commonly cause Tachydysrhythmias (sinus tachycardia, SVT, VT)?

A

Anticholinergics
Stimulants
Sympathomimetics

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30
Q

What drug ingestions can commonly cause QTc prolongation?

A

Antidepressants
Antidysrhythmic agents
Antipsychotic medications
Hydrofluoric acid
Many others

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31
Q

What drug ingestions can commonly cause ischemic changes on ECG?

A

Stimulants
Sympathomimetics

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32
Q

What are ECG findings of Digoxin?

A

Digitalis effect—seen in both therapeutic use and
overdose
Bidirectional VT (rare)
Atrial fibrillation with slow ventricular response

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33
Q

What ECG findings are common with Tricyclic antidepressants?

A

Rightward deviation of the QRS axis
Terminal R wave in aVR
QRS prolongation

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34
Q

What enzymes digest alcohol in the liver? What is the cofactor?

A

Alcohol Dehydrogenase
NAD+ is the cofactor

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35
Q

How does the metabolization of methanol and ethylene glycol differ from other types of alcohols?

A

the metabolites (not the parent compound) cause severe toxicity, making ADH blockade a key factor in treatment

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36
Q

What type of alcohol is seen in windshield wiper fluid, antifreeze, photocopier fluid, and solid fuels?

A

Methanol

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37
Q

What are the toxic metabolites of methanol?

A

Metabolized by ADH to a toxic metabolite, formaldehyde and then by aldehyde dehydrogenase (ALDH) to formic acid
Formic acid accumulation → anion gap metabolic acidosis.

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38
Q

What are the classic visual symptoms seen in methanol toxicity?

A

Classic description is “looking through a snow field,”
hyperemic optic discs, retinal edema (sluggish fixed pupils), blindness

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39
Q

How is methanol ingestion/toxicity diagnosed?

A

direct serum methanol measurement
(but serial bicarbonate measurements may be used if levels are not available)

Suspect methanol ingestion if patient has a high osmole gap, anion gap metabolic acidosis, and visual symptoms.

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40
Q

What osmole gap may suggest methanol ingestion/toxicity? and how is it calculated?

A

osmole gap > 10 mOsm/kg may be abnormal and may suggest the presence
of a toxic alcohol.
Osmole gap = measure osmolality − calculated
osmolarity, where calculated serum osmolarity = 2(Na+) + (BUN/2.8) + (glucose/18) + (ethanol/4.6).

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41
Q

What is the antidote for methanol ingestion/toxicity?

A

Fomepizole or ethanol

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42
Q

What is the mechanism of action of Fomepizole?

A

blocks ADH, preventing production of formic acid

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43
Q

How can you monitor response to treatment with fomepizole in someone with methanol ingestion/toxicity?

A

serial bicarbonate measurements

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44
Q

What is the role of Folate in the treatment of Methanol overdose/toxicity?

A

Folate improves the metabolism of formic acid to carbon dioxide and water.

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45
Q

When should hemodialysis be considered in methanol toxicity?

A

severe acidosis,
renal failure,
visual changes, or
a serum level ≥ 50 mg/dL

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46
Q

What toxic alcohol is most commonly found in engine coolants (antifeeze), break fluid?

A

Ethylene Glycol (OHCH2CH2OH)

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47
Q

How does Ethylene Glycol cause toxicity?

A

Ethylene glycol itself has minimal toxicity, causing mild intoxication.
■ Metabolized by ADH and ALDH to toxic metabolites: OXALIC ACID causes direct renal toxicity, and GLYCOLATE causes anion gap metabolic acidosis.

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48
Q

What are the 4 stages of ethylene glycol toxicity?

A

(1) acute neurologic stage (30 minutes to 12 hours);
(2) cardiopulmonary stage (12- 24 hours);
(3) renal stage (24-72 hours); and
(4) delayed neurologic sequelae (6-12 days)

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49
Q

How is ethylene glycol toxicity diagnosed?

A

Gold standard is direct serum measurement of ethylene glycol, or serial bicarbonate measurements if levels are not available

Suspect ethylene glycol ingestion if patient has an osmole gap, anion gap metabolic acidosis, and acute renal failure. Oxalic acid may also falsely
increase the serum lactate with some assays.

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50
Q

What is the antidote for ethylene glycol toxicity?

A

fomepizole or ethanol
(same as methanol)

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51
Q

Besides fomepizole or ethanol, what may be helpful in ethylene glycol toxicity?

A

Thiamine (vitamin B1) and pyridoxine (vitamin B6) may help convert glyoxylic acid to nontoxic metabolites.

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52
Q

When is HD indicated in ethylene glycol toxicity?

A

severe acidosis (pH < 7.25),
renal failure, or
electrolyte disturbances

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53
Q

What toxic alcohol is found in rubbing alcohol, perfumes, and some hand sanitizers?

A

ISOPROPANOL (ISOPROPYL A LCOHOL—CH3CHOHCH3 )

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54
Q

How does the metabolism of Isopropanol differ from that of methanol and ethylene glycol?

A

isopropanol is not metabolized to an organic acid. It is converted directly to acetone by ADH.

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55
Q

Isopropanol is directly toxic to __________.

A

GI mucosa

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56
Q

How is isopropanol toxicity diagnosed?

A

Measured directly in the serum
Ingestion should be suspected in patients who appear intoxicated but have low or undetectable ethanol levels.
Can get Osmolar gap, +serum acetone

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57
Q

How does isopropanol affect serum pH?

A

Isopropanol does NOT directly cause a metabolic acidosis. (whereas methanol and ethylene glycol do)

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58
Q

What is the treatment for isopropanol toxicity?

A

Supportive care only
(fomepizole will not help, HD will not help)

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59
Q

What 5 channels/receptors do TCAs affect?

A

Histamine receptors (blockade)
Muscarinic receptors (inhibition)
a-adrenergic receptors (blockade) –> hypotension
GABA receptor (antagonism) –>seizures
Na+ channel (blockade) –> QRS prolongation
K+ channel (antagonism) –> QTc prolongation

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60
Q

What are the early signs and symptoms of TCA poisoning?

A

Tachycardia, hypertension, rapid mumbled speech, urinary retention, alteration of consciousness

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61
Q

What are the late signs and symptoms of TCA poisoning?

A

Myocardial depression, hypotension, ECG with wide QRS >100 milliseconds → seizures, wide complex cardiac dysrhythmia.

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62
Q

How does acidosis worsen TCA overdose?

A

acidosis worsens sodium channel blockade –> increases QRS prolongation and seizures

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63
Q

What are ECG findings in TCA overdose?

A

QRS widening
>100 ms - associated with increased risk of seizures
>160 ms - associated with increased risk of wide complex dysrhythmias

Terminal R wave in aVr >3mm

Rightward deviation of the terminal 40 milliseconds of the QRS.

QTc prolongation

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64
Q

What is the treatment for TCA overdose?

A
  1. supportive; early intubation to avoid respiratory acidosis
  2. charcoal if within 1 hr of ingestion (intubate first)
  3. Sodium bicarb if indicated
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65
Q

What are indications for sodium bicarb administration in TCA overdose?

A

■ QRS > 120 milliseconds or longer
■ Ventricular dysrhythmias
■ Hypotension unresponsive to fluids
■ Administer boluses of 1-2 mEq/kg until narrowing of QRS

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66
Q

What is the mechanism of SSRIs?

A

Inhibition of presynaptic serotonin reuptake → increased CNS serotonin

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67
Q

What should you be thinking about in hyperthermic patient with AMS and myoclonus or rigidity?

A

Serotonin Syndrome

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68
Q

What is the treatment for SSRI (fluoxetine, citalopram, paroxetine) overdose?

A

Antidote = Cyproheptadine – use in Serotonin Syndrome in patient tolerating PO

Supportive care
Benzos for agitation, seizures, or neuromuscular hyperactivity

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69
Q

What are examples of medications that may cause MAO toxicity?

A

MAOIs: phenelzine, tranylcypromine, and St. John’s wort (supplement sometimes used for depression)

MAOI-B inhibitors (selegiline, rasagiline) are used to treat Parkinson disease and are much less toxic in overdose.

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70
Q

When is onset of symptoms with MAOI overdose?

A

6-12 hours delayed

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71
Q

What is the pathophysiology behind MAOI toxicity?

A

Inhibition of monoamine oxidase → decreased inactivation of biogenic amines, including epinephrine, norepinephrine, serotonin → excessive
circulating catecholamines

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72
Q

What are signs and symptoms of MAOI toxicity?

A

excessive sympathetic activity

■ Cardiovascular: Tachycardia, hyperthermia, hypertension
■ Musculoskeletal: Muscle rigidity, hyperreflexia, myoclonus
■ CNS: Seizures, coma, agitation, mydriasis

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73
Q

Describe the symptoms of a Tyramine reaction.

A

after ingestion of tyramine containing foods (red wine, cheese, etc)
■ Headache, hypertension, diaphoresis, palpitations, and neuromuscular excitation lasting for several hours

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74
Q

What is the treatment for MAOI toxicity?

A

Benzos for: agitation, rigidity, seizures, tachycardia, hyperthermia
If severely hypertensive –> sodium nitroprusside or phentolamine

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75
Q

What is the hallmark of bupropion toxicity?

A

seizures

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76
Q

What are hallmarks of mirtazepine (remeron) toxicity?

A

hypotension, serotonin syndrome

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77
Q

What are hallmarks of Trazodone toxicity?

A

Similar to SSRIs
Serotonin syndrome
Hypotension
Priapism

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78
Q

What are hallmarks of Venlafaxine toxicity?

A

CNS sedation
Serotonin syndrome
Dysrhythmias
Seizures

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79
Q

What 3 conditions are associated with chronic use of Isoniazid?

A

peripheral neuropathy
hepatitis
drug-induced systemic lupus erythematosus (SLE)

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80
Q

How does Isoniazid cause toxicity?

A

Reduction of vitamin B6 in brain → ↓ GABA production (the inhibitory neurotransmitter
in the brain) but ↑glutamate (the excitatory neurotransmitter in the brain) → seizures

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81
Q

What is the treatment for Isoniazid toxicity?

A

Pyridoxine (Vitamin B6) - replenished Vitamin B6 stores to help replete GABA
AC if early and no CNS depression
Barbiturates and benzodiazepines for status epilepticus until antidote available.

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82
Q

What is a complication of chronic large doses of pyridoxine?

A

peripheral neuropathy

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83
Q

How do reverse transcriptase inhibitors cause toxicity?

A

Mitochondrial toxicity → lactic acidosis, hepatotoxicity, pancreatitis

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84
Q

What are symptoms of reverse transcriptase inhibitor toxicity?

A

■ Malaise
■ Tachypnea, hyperpnea
■ Nausea/vomiting, abdominal pain

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85
Q

What is the treatment for toxicity caused by Reverse Transcriptase Inhibitor Toxicity?

A

If severe lactic acidosis → sodium bicarbonate, HD, or CRRT for correction of acidosis

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86
Q

In addition to anticholinergic toxidrome, what channel blockade may be seen with diphenhydramine overdose?

A

Sodium channel blockade
ie QRS prolongation

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87
Q

What is the treatment for anticholinergic toxicity?

A

IV fluids and benzos (for seizures, agitation, and hyperthermia)
Antidote = physostigmine
&raquo_space; indicated for agitation and delirium uncontrolled with sedatives
» contraindicated if QRS >100 ms or hx of TCA overdose

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88
Q

What is the mnemonic for cholinergic toxidrome?

A

SLUDGE
Salivation/Sweating
Lacrimation
Urination
Defecation
Gastrointestinal distress
Emesis

plus

“The Killer Bs”
Bradycardia
Bronchorrhea
Bronchospasm

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89
Q

What can be a complication of anticholinergic toxicity?

A

Rhabdomyolysis – may need to follow CK and Creatinine

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90
Q

What agents may cause cholinergic toxicity?

A

Donepezil
Pyridostigmine
edrophonium
organophosphates
Sarin (nerve agent used in bioterrorism)
Pilocarpine (used in glaucoma)
Nicotine
Muschrooms (Clytocybe and inocybe species)

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91
Q

What is the mechanism of cholinergic toxicity?

A

Inhibition of the enzyme acetylcholinesterase → excess acetylcholine at muscarinic and nicotinic receptors

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92
Q

What are signs/symptoms of cholinergic toxicity?

A

AMS (delirium to coma), seizures, lacrimation, salvation, sweating, bronchorrhea, bronchospasm, bradycardia, miotic (constricted) pupils, urinary/bowel incontinence, hyperactive bowel sounds, and muscle fasciculations

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93
Q

What is the treatment for cholinergic toxicity

A

Supportive care:
1. Atropine to dry up airway secretions and treat unstable bradycardia (very high doses often needed),
2. benzodiazepines for seizures
and agitation, and
3. pralidoxime (2-PAM) to regenerate acetylcholinesterase in organophosphate poisoning

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94
Q

Describe the onset and timing of warfarin overdose.

A

effect is delayed typically >/=15 hours
duration of action may be up to 6 days

(PT/INR should be monitored for 3-4 days)

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95
Q

What is the mechanism of action of warfarin?

A

Blocks the synthesis of antithrombotic proteins C and S → prothrombotic period before vitamin K–dependent factors are depleted

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96
Q

What is the treatment for Warfarin overdose?

A

Activated charcoal if within 1 hour
supportive with pRBCs if needed

Approach depends on INR for Vitamin K, FFP, PCC, recombinant factor VIIa

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97
Q

Warfarin: What is the treatment for INR <5 without any clinically significant bleeding?

A

lower or skip dose; resume when INR therapeutic

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98
Q

Warfarin: What is the treatment for INR 5-9 without any clinically significant bleeding?

A

omit 1-2 doses
OR
skip dose and give vitamin K1 (1-2mg PO)
resume at lower dose when INR therapeutic

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99
Q

Warfarin: What is the treatment for INR >9 without any clinically significant bleeding?

A
  1. Hold Warfarin
  2. Give higher dose of Vitamin K1 (5-10mg PO)
  3. Resume at lower dose when INR therapeutic
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100
Q

Warfarin: What is the treatment for serious bleeding at any elevation of INR?

A
  1. Hold Warfarin
  2. Give Vitamin K (10mg slow IV
  3. Give FFP or PCC
    (recombinant factor VIIa is an alternative therapy)
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101
Q

On Warfarin: What is the treatment for life threatening bleeding?

A
  1. Hold Warfarin
  2. Give Vitamin K (10mg slow IV
  3. Give FFP, PCC, or recombinant factor VIIa
    Repeat as necessary
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102
Q

What is the dose for FFP?

A

10-15 mg/kg will restore factor levels to ≥ 30% of normal

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103
Q

What is a risk factor for Warfarin-induced skin necrosis?

A

protein C deficiency

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104
Q

What is the mechanism of warfarin-induced skin necrosis?

A

transient hypercoagulable state leading to thrombosis of cutaneous vessels (most commonly 3-8 days after initiating warfarin)

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105
Q

How can warfarin induced skin necrosis be avoided?

A

Prevented by coadministration of heparin during initiation of warfarin therapy

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106
Q

How is warfarin induced skin necrosis treated?

A

discontinuation of warfarin and initiation of heparin therapy

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107
Q

What is the mechanism of Heparin toxicity?

A

Binds antithrombin III → heparin-antithrombin III complex → inhibits multiple steps (IXa, Xa, XIa, XIIa, and thrombin) in intrinsic and extrinsic pathways

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108
Q

What is the treatment for Heparin/LMWH toxicity?

A

antidote = protamine sulfate

Indicated for severe bleeding complications only (risk of serious anaphylaxis with administration) and reverses the effect of heparin (only partially inactivates LMWH)

109
Q

When is heparin induced thrombocytopenia (HIT) most likely to occur?

A

May occur 5-10 days after initiating therapy or as late as 3 weeks after stopping therapy

110
Q

What are signs and symptoms of heparin-induced thrombocytopenia?

A

Antibodies cause significant drop in platelets (> 50%) and skin changes at injection sites.
Systemic venous and arterial thrombotic events can cause a wide variety of end organ damage.

(This is more common with heparin than LMWH.)

111
Q

How do phenytoin, carbamazepine, topiramate, and valproic acid cause toxicity?

A

Sodium channel blockade

112
Q

How does Gabapentin and pregabalin cause toxicity?

A

Calcium channel blockade

113
Q

Why does phenytoin cause cardiac toxicity?

A

Rapid IV infusion of phenytoin → myocardial depression and cardiac arrest from propylene glycol diluent (not present in fosphenytoin)

114
Q

What is the mechanism of action of phenobarb toxicity?

A

GABA agonism

115
Q

What are the symptoms of mild Carbamazepine toxicity?

A

ataxia and nystagmus

116
Q

What are the symptoms of severe Carbamazepine toxicity?

A

seizures, respiratory and CNS depression, and dysrhythmias (AV block, QRS/QTc prolongation)

117
Q

What Carbamazepine level may correlate with severe toxicity?

A

serum concentrations >40 mg/L

118
Q

What are symptoms of mild to moderate Phenytoin toxicity?

A

Nystagmus, ataxia, and dysarthria

119
Q

What are symptoms of severe Phenytoin toxicity?

A

stupor, coma, respiratory arrest

120
Q

What serum concentrations may correlate with severe phenytoin toxicity?

A

serum concentrations >50 mg/L

121
Q

What signs/symptoms may occur with rapid IV injection of phenytoin?

A

hypotension, bradycardia, and cardiac arrest due
to diluent (propylene glycol)

122
Q

What is purple glove syndrome?

A

Serious soft tissue reaction to phenytoin
- Edema, pain, ischemia, tissue necrosis, compartment syndrome

123
Q

What are symptoms of mild to moderate Valproic acid toxicity?

A

nausea, vomiting, CNS depression

124
Q

What are symptoms of severe Valproic acid toxicity?

A

Coma, respiratory depression, seizures,
metabolic disturbances, cardiac arrest

125
Q

What serum level may correlate with severe valproic acid toxicity?

A

level > 850 mg/L

126
Q

How long should anti-epileptic overdoses be observed?

A

at least 6 hours – however peak serum concentrations may be delayed with ingestion of modified-release products.

127
Q

What is the treatment for anti-epileptic overdoses?

A

Activated charcoal in patients presenting early without CNS depression
■ MDAC increases the clearance of phenytoin, carbamazepine, and
phenobarbital.

128
Q

What can be used to treat valproic acid induced hyperammonemia?

A

L-carnitine

129
Q

What hypersensitivity reaction is associated with anti-epileptics?

A

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome
Initial symptoms include fever, malaise, pharyngitis with progression to drug rash, lymphadenopathy, and multiorgan involvement with fatality rates as high as 10%.

130
Q

What physical exam finding can be seen in chronic phenytoin therapy?

A

Gingival hyperplasia

131
Q

What is the treatment for gabapentin OD?

A

supportive, AC

132
Q

What are the signs/symptoms of Lamotrigine overdose?

A

Nausea, vomiting, lethargy, ataxia, nystagmus, seizures, coma QRS widening/ventricular dysrhythmias

133
Q

What is the treatment for Lamotrigine overdose?

A

ortive, AC, benzodiazepines for seizures, sodium bicarbonate
for QRS prolongation

134
Q

What are the signs/symptoms of Levetiracetam OD?

A

Lethargy, coma, and respiratory depression, and rarely psychosis

135
Q

What is the treatment for Keppra OD?

A

supportive, AC

136
Q

What are the signs/symptoms of Oxcarbazepine (Trileptal) OD?

A

Somnolence, tinnitus, bradycardia, and ↓ BP

137
Q

What is the treatment for Oxcarbazepine (Trileptal) OD?

A

Supportive, AC

138
Q

What are the signs/symptoms of Tiagabine (Gabitril) OD?

A

Lethargy, facial myoclonus (grimacing), nystagmus, posturing, coma, and seizures (stimulation of GABAB receptors on thalamus)

139
Q

What is the treatment of Tiagabine (Gabitril) OD?

A

Supportive, AC; seizures, posturing, or grimacing with benzodiazepines as first line

140
Q

What is the mechanism of toxicity of Topiramate?

A

Inhibits carbonic anhydrase causing a nongap acidosis, renal tubular acidosis (renal tubular acidosis [RTA]—↑ urine pH), hypokalemia, and
hyperchloremia

141
Q

What are the signs/symptoms of Topiramate OD?

A

Nephrolithiasis, lethargy, ataxia, nystagmus, echolalia, psychosis, hallucinations, myoclonus, waxing and waning lucid intervals,
myopia, acute angle glaucoma, coma, seizures, and status epilepticus

142
Q

What is the treatment of Topiramate OD?

A

Supportive, AC, sodium bicarbonate (1-2 mEq/kg) for severe RTA, and rarely HD

143
Q

Parkinson disease is a neurodegenerative disorder affecting the ______ resulting in reduced production of _______, an essential neurotransmitter for the control of movement and coordination.

A

substantia nigra,
dopamine

144
Q

What is the mechanism of toxicity of Levodopa and dopamine agonists?

A

Excessive activation of dopaminergic
neurons and activation of serotonergic systems

145
Q

What is the mechanism of toxicity of COMT inhibitor and monoamine oxidase B inhibitor?

A

Excessive circulating catecholamines

146
Q

What is the mechanism of toxicity of amantadine and anticholinergics?

A

Inhibition of central and peripheral
muscarinic receptors

147
Q

What are symptoms of ACUTE toxicity from Levodopa and dopamine agonists?

A

Anxiety, confusion, agitation, tachycardia, orthostatic hypotension, nausea/vomiting, dyskinesias

148
Q

What are symptoms of CHRONIC toxicity from Levodopa and dopamine agonists?

A

Dystonia, hallucinations, hypersexuality, delusions, fibrotic changes (dopamine agonists only)

149
Q

What are symptoms of toxicity from Amantadine and anticholinergics?

A

Agitation/confusion, hallucinations,
hyperthermia, tachycardia, dry mucous membranes, decreased bowel
sounds, and urinary retention

150
Q

______ is metabolized to l-methamphetamine, which can be detected on urine toxicology screening.

A

Selegiline

151
Q

Therapeutic effects of antipsychotics are
due to antagonism of ______ _______ receptors

A

mesolimbic dopamine

152
Q

What are signs and symptoms of antipsychotic overdose?

A

■ Nonspecific dopamine receptor antagonism → extrapyramidal symptoms and neuroleptic malignant syndrome (NMS)
■ α1-Adrenergic antagonism → hypotension and reflex tachycardia
■ Muscarinic receptor antagonism → anticholinergic symptoms
■ Histamine receptor antagonism → sedation
■ Cardiac fast sodium channel blockade → QRS widening
■ Cardiac K+ channel blockade → prolonged QTc

153
Q

What are four typical antipsychotics?

A

Haloperidol, droperidol
Chlorpromazine
Fluphenazine

154
Q

What are 4 Atypical antipsychotics?

A

Risperidone (Risperdal)
Quetiapine (Seroquel)
Olanzapine (Zyprexa)
Aripiprazole (Abilify)

155
Q

What is the treatment for beta blocker overdose?

A

If bradycardic and hypotensive:
1. IVF
2. Atropine
3. Pressors
4. Calcium
5. High dose glucagon (5-10mg)
6. High dose insulin (increases cardiac output)
- start at 1 unit/kg then drip at 1 unit/kg/hr and titrate
- consider dextrose bolus and infusion to maintain blood glucose 100-200 mg/dL

■ Cardiac pacing, intra-aortic balloon pump, and bypass should be considered
if pharmacologic measures fail.
■ Sodium bicarbonate for prolonged QRS in propranolol toxicity.
■ HD may be considered for atenolol toxicity.

156
Q

Hyperglycemia is suggestive of
_________ overdose in
the undifferentiated hypotensive and
bradycardic patient.

A

calcium channel blocker

157
Q

What is the treatment for calcium channel blocker overdose?

A

Same as that for beta blocker overdose, but glucagon less likely to help

158
Q

What is the mechanism of action of Digoxin?

A

■ Inactivation of the Na+/K+ ATPase pump on the cardiac cell membrane → increased intracellular Ca++ and extracellular K+
■ Increased automaticity
■ Decreases conduction through the AV node via increased vagal tone

159
Q

In Digoxin overdose, ____ in acute toxicity is a predictor of poor outcome without
treatment.

A

Hyperkalemia

160
Q

______ may enhance chronic toxicity → toxicity at lower digoxin levels.

A

Hypokalemia

161
Q

What are the signs/symptoms of Digoxin toxicity?

A

CV: Acute toxicity → more bradycardia and blocks, chronic toxicity → ventricular dysrhythmias more common
GI: n/v, anorexia
Neuro: visual disturbances (scotomata, yellow halos around lights), headache, weakness, AMS

162
Q

Monitoring of what two things is essential for anyone prescribed digoxin?

A

potassium and renal function monitoring

163
Q

Bidirectional VT is fairly specific for _______ toxicity.

A

cardiac glycoside (digoxin)

164
Q

What is the treatment for digoxin toxicity?

A
  1. K+ and Mag repletion
  2. Treat bradycardia with Atropine and/or pacing
  3. tachydysrhythmias –> tx with phenytoin and lidocaine
  4. Antidote = digoxin-specific antibodies
165
Q

Why should you avoid cardioversion an defibrillation in digoxin toxicity?

A

may induce VT/VF (ventricular fibrillation).
■ Phenytoin and lidocaine are felt to be safest drugs.
■ Phenytoin can increase AV nodal conduction.

166
Q

What is the dose for digoxin specific antibodies for acute toxicity (empiric dosing, serum concentration unknown)?

A

10-20 vials

167
Q

What is the dose for digoxin specific antibodies for chronic toxicity in adults?

A

2-4 vials

168
Q

What is the dose for digoxin specific antibodies for chronic toxicity in children?

A

1-2 vials

169
Q

What is the mechanism of Clonidine toxicity?

A

Central presynaptic α2-adrenergic agonist → decreased sympathetic (norepinephrine)
outflow → hypotension and bradycardia.

Peripherally, presynaptic α2-agonism may result in vasoconstriction and
paradoxical transient hypertension.

170
Q

What are the signs and symptoms of Clonidine overdose?

A
  1. Initial, short-lived hypertension progresses to hypotension and bradycardia
  2. Hypoventilation
  3. Mental status depression, coma, and miosis
171
Q

what is the treatment for clonidine overdose?

A

supportive
IV fluids +/- atropine, vasopressors
+/- naloxone

172
Q

List 3 sulfonylurea medications?

A

Glipizide, Glyburide, Glimepiride

173
Q

What is the mechanism of sulfonylurea toxicity?

A

↑ Secretion of preformed insulin from pancreatic β-islet cells → hypoglycemia.

174
Q

What is the treatment for sulfonylurea overdose?

A

■ AC if recent ingestion and protected airway
■ Correct hypoglycemia with dextrose boluses as needed to maintain normal
serum glucose
■ Antidote = octreotide
NEED 24 HOUR OBS

175
Q

What is the mechanism of action of octreotide (with respect to sulfonylurea overdose)

A

Long-acting synthetic analog of somatostatin, inhibits release of insulin from pancreas

176
Q

____________ (headache, flushing, nausea/vomiting) are possible with
all sulfonylureas following exposure to alcohol

A

Disulfiram reactions

177
Q

When is the onset of action of symptoms with levothyroxine (t4) overdose?

A

may be delated 2-5 days

178
Q

What is the treatment for levothyroxine overdose/toxicity?

A

■ AC if presenting within 1-2 hours of large acute ingestion may prevent
later toxicity.
■ Benzodiazepines for agitation.
■ β-Antagonists, such as propranolol or esmolol, to control severe tachydysrhythmias.

(Agents that block endogenous thyroid hormone production (PTU, methimazole)
have limited utility)

179
Q

when should endoscopy occur for caustic ingestions?

A

within 24 hours or delay for 2 weeks

180
Q

Where can hydrogen fluoride be found?

A

rust removers, oven cleaners, and automotive wheel cleaners.
glass etching, graffiti removal, and manufacture of semiconductors and certain
fuels

181
Q

what are signs and symptoms of hydrogen fluoride toxicity?

A

Pain at site of exposure
hypocalcemia, hypomagnesemia
hyperkalemia due to cellular breakdown

182
Q

How is pain from hydroflouric acid treated?

A

Calcium gluconate paste

183
Q

How do adults typically get exposed to lead?

A

primarily occupational (construction,
mining, welding, smelting, manufacture of batteries, plastic and rubber, “moonshine”)

184
Q

How do children typically get exposed to lead?

A

accidental ingestion of lead-containing material, especially paint chips, imported toys and jewelry

185
Q

What are signs and symptoms of chronic lead toxicity?

A

Subtle, insidious, and nonspecific symptoms,
including headache, peripheral motor neuropathy (wrist drop), HTN, anemia,
gout, and cognitive impairment

186
Q

What are signs and symptoms of acute lead toxicity?

A

■ Nausea/vomiting, constipation, abdominal pain (lead colic)
■ Anemia
■ Encephalopathy, ataxia, and seizures

187
Q

What is the treatment for lead toxicity, where ingestion is visible on XR?

A

whole bowel irrigation

188
Q

What is the treatment for severe lead toxicity (encephalopathy or lead level >100 ug/dL)?

A

Chelators = BAL (British anti-lewisite, dimercaprol) and Ca-EDTA

Treat with BAL first then follow with Ca-EDTA for encephalopathy

189
Q

What should be administered in child with lead level >45 or adults with lead level >80 regardless of symptoms?

A

Chelator = DMSA (2,3-dimercaptosuccinic acid, succimer) oral chelation therapy

190
Q

In what products would you find arsenic?

A

Pesticides, wood preservatives, metal alloys, chemical synthesis, and glass manufacturing, folk remedies.

(Arsenic trioxide is used as a chemotherapeutic agent for acute promyelocytic leukemia.)

191
Q

What are symptoms of chronic arsenic poisoning?

A

■ Peripheral neuropathy, headache, ataxia, confusion, malaise
■ Hyperpigmentation, Mees lines (transverse white lines on nails), alopecia
■ Skin lesions: Hyperkeratotic lesions palms and soles
■ Cancer: Skin, lung, bladder

192
Q

What are symptoms of acute arsenic poisoning?

A

■ GI symptoms predominate: Violent gastroenteritis
■ Confusion, coma, seizures
■ Hypotension, tachycardia, prolonged QTc interval, torsade de pointes
■ ARDS

193
Q

What are signs/symptoms of Arsine gas poisoning?

A

■ Findings consistent with acute hemolysis: Hematuria, jaundice, renal failure
■ Abdominal pain, nausea/vomiting
■ Hypotension, tachycardia, pulmonary edema
■ Symptoms may be delayed 2-24 hours

194
Q

How is arsenic poisoning diagnosed?

A

24 hours urine arsenic levels
(blood levels not useful)

195
Q

What are signs/symptoms of mercury toxicity?

A

Elemental mercury (inhaled) → respiratory distress.
Inorganic mercury (ingested) → severe corrosive gastroenteritis.
Organic mercury (ingested) → delayed neurotoxicity.

196
Q

What is the treatment for mercury toxicity?

A

■ WBI: If radiopaque objects visible on x-ray
■ Antidote = BAL (British anti-lewisite, dimercaprol) if severe GI symptoms
or
DMSA (2,3-dimercaptosuccinic acid, succimer) if able to tolerate PO

197
Q

What are common sources of CO?

A

vehicle exhaust, ovens, house fires, furnaces,
and portable generators

198
Q

What is the mechanism of CO toxicity?

A

Binds to hemoglobin → carboxyhemoglobin (COHb) incapable of carrying O2 → impaired O2 delivery, cellular hypoxia, lactic acidosis

199
Q

Carbon monoxide shifts the oxyhemoglobin dissociation curve to _____ → ↓ release of O2 to
tissues from normal hemoglobin

A

left

200
Q

How is carbon monoxide poisoning diagnosed?

A

Direct measurement of COHb in either arterial or venous blood via
co-oximetry.
■ Normal nonsmoker = 2%-3%
■ Smokers = < 10

201
Q

What is the elimination half life of CO on room air, 100% O2 and hyperbaric O2?

A

Room air: 4-5 hours
100% O2: 1-1.5 hour
Hyperbaric O2: 20-30 minutes

202
Q

What are possible sources of Cyanide toxicity?

A

■ Combustion of plastics, synthetic fibers, or wool; house fires (smoke inhalation)
represent the most likely source of exposure.
■ Prolonged infusion of nitroprusside.
■ Industry including mining, plastics manufacturing, welding, fumigation,
chemical synthesis, and research.
■ Pits and seeds of certain fruits (apricots, bitter almonds) contain amygdalin,
which releases CN in vivo during its metabolism.

203
Q

With what toxicity, does a patient have a distinctive bitter almond-like odor?

A

Cyanide toxicity

204
Q

What 3 components make up a cyanide antidote kit?

A

■ Amyl nitrite pearls (for inhalation, prior to IV access)
■ Sodium nitrite (IV)
■ Sodium thiosulfate (IV)

205
Q

Instead of the cyanide antidote kit, what other antidote can be given for cyanide toxicity?

A

hydroxycobalamin (Vitamin B12)
(actually becoming preferred)

206
Q

What are notable side effects from Hydroxycobalamin administration?

A

causes body fluids to become red and causes transient hypertension

207
Q

What are possible sources of hydrogen sulfide (H2S) exposure?

A

■ Sewer or manure gas
■ Chemical or industrial processes, such as tanning, rubber vulcanizing, mining, and manufacture of paper, silk, rayon, refrigerants, soap, and petroleum products
■ Natural sources include hot springs and volcanic eruptions

208
Q

What two toxicities should be considered in any patient with rapid onset of coma, shock, and marked lactic acidosis?

A

CN and H2S

209
Q

What is the treatment for Hydrogen Sulfide toxicity?

A

100% O2
if prolonged sx –> sodium thiosulfate

(observe for several hours for delayed onset pulmonary edema)

210
Q

What are the signs/symptoms of acute lithium ingestion?

A

GI toxicity > > CNS toxicity (no time for CNS uptake)
■ GI toxicity = nausea/vomiting/diarrhea
■ CNS findings are typically mild, but can develop over hours and include
hyperreflexia, tongue fasciculations, clonus, agitation, AMS, seizures

211
Q

What are the signs/symptoms of chronic lithium ingestion?

A

CNS toxicity > > GI toxicity.
■ CNS effects may range from lethargy and confusion to coma and seizures.
■ ECG changes include T-wave inversions, T-wave flattening, depressed ST segments, and less commonly bradycardia and sinus node arrest.

212
Q

How is lithium toxicity diagnosed?

A

Clinical diagnosis based on history and examination

Lithium levels:
■ Measure 4-6 hours postingestion, follow levels until clear peak and decline
■ Peak serum level with large ingestion, especially sustained-release preparations,
may occur > 12 hours postingestion

213
Q

What is the treatment for Lithium overdose

A

hydration
Hemodialysis
benzos for seizures and agitation

214
Q

What are 4 complications of lithium toxicity?

A
  1. hypothyroidism
  2. nephrogenic DI
  3. increased risk of serotonin syndrome
  4. Syndrome of irreversible lithium-effectuated neurotoxicity (SILENT): Irreversible neurologic and neuropsychiatric sequelae
215
Q

______ is more cardiotoxic than other local anesthetics and is not indicated for IV regional anesthesia.

A

Bupivacaine

216
Q

Which two local anesthetics can cause methemoglobinemia?

A

benzocaine and prilocaine

217
Q

What is the treatment for local anesthetic toxicity?

A

IV fat emulsions (Intralipid), acts as a lipid sink pulling local anesthetics away from site of toxicity, given as a 20% solution 1.5-mL/kg
bolus followed by 0.25 mL/kg/min over 30-60 minutes

218
Q

What 3 drugs are considered methylxanthines?

A

Caffeine, theophylline, theobromine

219
Q

What are signs/symptoms of Vitamin A overdose?

A

Headache, papilledema, photophobia, seizures, psychosis, nausea/vomiting, abdominal
pain, liver injury, desquamation.
Hypercarotenemia causes yellow-orange
discoloration of skin

220
Q

What are signs/symptoms of Vitamin D overdose?

A

Hypercalcemia

221
Q

What are signs/symptoms of Vitamin E overdose?

A

Nausea/vomiting, diarrhea, abdominal cramps, coagulopathy

222
Q

What are adverse effects of anabolic steroids?

A

increase cancer risk,
increased risk of MI, VTE, and cardiac death
acne, stray and gynecomastia
peliosis hepatis (blood filled sinuses in the liver)
immunosuppression
tendon and ligament rupture
mood lability, psychosis

223
Q

An ingestion of > _____ mg/kg (children) or ____ g (adults) in less than an 8-hour period should
be considered potentially toxic

A

150 mg/kg
7.5 g

224
Q

What is the toxic metabolite of acetaminophen?

A

N-acetyl-p-benzoquinone imine (NAPQI)

225
Q

Hepatic stores of ___________ rapidly combine with NAPQI to form nontoxic metabolites.

A

glutathione

226
Q

Which patient populations are at higher risk for acetaminophen toxicity?

A

Patients with decreased glutathione stores (alcoholics, malnourished) and those on cytochrome P450–inducing medications
(INH, anticonvulsants) may have increased risk of hepatotoxicity

227
Q

What is a potentially toxic dose of acetaminophen in patients <6 years old?

A

≥ 200 mg/kg over 24 hours

228
Q

What is a potentially toxic dose of acetaminophen in patients >6 years old?

A

≥ 10 g or 200 mg/kg (whichever is less)
over 24 hours

229
Q

If time of tylenol ingestion is unknown, what tylenol level should you administer NAC?

A

If the APAP level is > 20 µg/mL or the AST/ALT is elevated → treat with NAC.

230
Q

If the patient’s serum APAP concentration is above _____ mg/mL at 4 hours postingestion), start treatment with N-acetylcysteine (NAC)

A

150 mg/mL

231
Q

What is the dose of NAC?

A

■ Oral (Mucomyst): 140 mg/kg load, then 70 mg/kg every 4 hours for 72 hours.
■ IV (Acetadote): 150 mg/kg load, then 12.5 mg/kg/h × 4 hours, then 6.25 mg/kg/h × 16 hours.

232
Q

What are indications for liver transplantation in tylenol overdose?

A

Indications for liver transplantation (King’s College Criteria) include:
1. pH < 7.3 after resuscitation, or
2. all 3 of INR > 6.5,
3. creatinine > 3.4 mg/dL,
4. grade 3 or 4 encephalopathy

233
Q

What is the mechanism of ASA toxicity?

A

■ Direct stimulation of respiratory center → hyperventilation, respiratory alkalosis
■ Stimulation of chemoreceptor trigger zone → vomiting
■ Uncoupling of oxidative phosphorylation → anaerobic metabolism, anion-gap metabolic acidosis, hyperthermia
■ Permanent inhibition of platelet aggregation
■ Ototoxicity → tinnitus and hearing loss correlate with salicylate level
■ Alterations in capillary integrity → cerebral and pulmonary edema

234
Q

What are early signs of ASA toxicity?

A

Nausea/vomiting, tinnitus, hearing loss, lethargy, hyperventilation,
diaphoresis, and hyperthermia

Mixed acid-base picture with a respiratory alkalosis and anion-gap metabolic acidosis
■ Blood gases early in toxicity often show a respiratory alkalosis with pH > 7.5

235
Q

What is the treatment for ASA toxicity?

A

Sodium bicarbonate therapy:
■ 1- to 2-mEq/kg IV bolus, followed by drip
■ Goal is urinary alkalinization to pH 7.5-8.0

236
Q

What electrolyte disturbance is common in ASA toxicity?

A

Hypokalemia (due to intracellular shifts and body losses)
(Urinary alkalinization will not occur unless hypokalemia is corrected)

237
Q

How often should you obtain ASA levels?

A

q1-2 hrs

238
Q

What is the mechanism of action of NSAIDs?

A

inhibit the enzyme cyclooxygenase,
causing decreased prostaglandin formation

239
Q

Symptomatic overdose occurs with ibuprofen ingestion >____ mg/kg

A

200

240
Q

What are signs and symptoms of NSAID toxicity?

A

■ GI: Nausea, vomiting, gastritis, upper GI bleed
■ Renal: Renal insufficiency due to decreased renal blood flow; more common
in chronic than acute exposure
■ anion gap metabolic acidosis
■ Systemic: May be seen with massive ibuprofen overdose; symptoms
include cerebral and pulmonary edema, seizures, coma

241
Q

What is the treatment for NSAID toxicity?

A

supportive and symptomatic therapy

242
Q

What are the five phases of Iron Toxicity?

A

Phase 1: GI phase
Phase 2: Latent phase
Phase 3: ”Shock” phase
Phase 4: Fulminant hepatic failure
Phase 5: Delayed sequelae

243
Q

What is a toxic dose of elemental iron?

A

> 20 mg/kg

244
Q

What is the mechanism of iron toxicity?

A

Direct corrosive effect on GI tract
Toxicity from free circulating iron → cellular uncoupling of oxidative phosphorylation and production of free radicals → anaerobic metabolism and multi-organ failure

245
Q

How long should iron overdose be monitored for sx?

A

6 hours
If not vomiting within 6 hours – no toxicity

246
Q

What serum iron concentration indicates severe toxicity?

A

Total serum iron concentration at 4-6 and 6-8 (for sustained-release or enteric-coated preparations, respectively) hours postingestion.
■ Iron concentration > 500 mg/dL = severe toxicity.

247
Q

What is the antidote for iron toxicity and what are the indications for it?

A

Deferoxamine
1. systemic illness (severe acidosis, shock)
2, serum iron levels > 500 ug/dL (with clinical sx)

248
Q

What is a side effect of deferoxamine administration for iron toxicity?

A

Renally excreted deferoxamine-iron complexes may cause urine color to pink-red (“vin-rose”).

249
Q

What is the mechanism of Dextromethorphan toxicity?

A

Antagonizes N-methyl-d-aspartate (NMDA) receptors (similar to ketamine or phencyclidine [PCP]), inhibits serotonin reuptake, and at high doses, acts as an agonist at opioid receptors

250
Q

What are symptoms of mild to moderate dextromethorphan overdose?

A

Agitation, ataxia, nystagmus, visual and
auditory hallucinations.

251
Q

What are symptoms of severe dextromethorphan overdose?

A

Coma and respiratory depression

252
Q

What is the mechanism of diphenhydramine toxicity?

A

■ H1-receptor antagonism → smooth muscle relaxation, sedation
■ Muscarinic receptor antagonism → anticholinergic toxidrome
■ Na+ channel blockade (at high doses) → QRS prolongation, seizure

253
Q

What are the signs/symptoms of diphenhydramine toxicity?

A

■ CNS depression.
■ Anticholinergic toxidrome.
■ Extremely large doses may cause seizures and dysrhythmias.

254
Q

What is the treatment for diphenhydramine toxicity?

A

■ Supportive and symptomatic therapy
■ Benzodiazepines for agitation or seizures
■ Sodium bicarbonate if QRS prolongation or wide complex dysrhythmias

255
Q

What is the mechanism of toxicity of organophosphates and carbamates?

A

■ Inhibition of cholinesterase → increases synaptic acetylcholine → increased activity at all nicotinic and muscarinic receptors.

■ Carbamates bind cholinesterase transiently (minutes to hours).
■ Organophosphates can undergo “aging” → irreversible binding of the insecticide to cholinesterase.

256
Q

What is the treatment for Organophosphate toxicity?

A
  1. decontamination
  2. airway monitoring, benzos for seizures
  3. antidotes = atropine, pralidoxime (2-PAM)
257
Q

When should atropine be given for organophosphate poisoning and what is the end goal?

A

used for hemodynamically unstable bradycardia and excessive secretions

endpoint is drying of airway secretions

258
Q

What is the dose of atropine for organophosphate poisoning?

A

Very high doses often needed; 0.5-2 mg IV initially with doubling of dose every 5 minutes until drying of airway secretions

259
Q

What is the mechanism of action of pralidoxime (2-PAM)?

A

used to reactivate inhibited cholinesterase
in organophosphate poisoning prior to “aging”

260
Q

What is strychnine?

A

rodentacide

261
Q

What are signs/symptoms of strychnine poisoning?

A

rapid onset involuntary muscle contractions,
opisthotonus, hyperreflexia, clonus, and trismus usually within 15-30 minutes of ingestion.
■ Mental status is not affected

262
Q

What is the treatment for strychnine toxicity?

A

■ Benzodiazepines or barbiturates are administered to relieve excessive muscular
activity.
■ More severe cases may require intubation and neuromuscular blockade.

263
Q

What is the mechanism of barbiturate toxicity?

A

■ Binds to GABAA chloride channel → increased duration of channel opening,
depression of neuronal firing
■ Depresses medullary respiratory centers
■ Inhibits myocardial contractility and conduction

264
Q

What are the signs/symptoms of mild to moderate barbiturate toxicity?

A

Lethargy, nystagmus, ataxia, slurred speech
(similar to alcohol intoxication)

265
Q

What are the signs/symptoms of severe barbiturate toxicity?

A

Small/midsized pupils, hypothermia, coma, respiratory depression, hypotension, bradycardia

266
Q

What is the treatment for severe barbiturate toxicity?

A

■ Supportive therapy.
■ MDAC may be beneficial in phenobarbital overdose only if airway is protected.
■ WBI if large ingestion of long-acting agents only if conditions are appropriate.
■ HD for severely intoxicated patients refractory to above therapy.

267
Q

What is the mechanism of Benzodiazepine toxicity?

A

■ Enhanced binding of GABA to GABA-A channels → depression of neuronal firing
■ Toxicity limited by availability of GABA and hence safer in overdose then barbiturates.
■ Peripheral vasodilatation

268
Q

What are symptoms of benzo overdose?

A

■ Mild to moderate intoxication: Lethargy, slurred speech, ataxia
■ Severe intoxication: Coma, respiratory depression

269
Q

How is benzo overdose treated?

A

supportive therapy
Flumazenil
- Limited utility in the ED: Mostly for reversal of procedural sedation, whereas routine use in acute overdose is not recommended because
benzodiazepine overdose alone is rarely fatal, may have significant side effects especially in benzodiazepine-dependent patients.

270
Q

How are sympathomimetic toxidromes differentiated from anticholinergic toxidromes?

A

Diaphoretic, not dry, skin and hyperactive,
not hypoactive, bowel sounds are the key
to differentiating the sympathomimetic
toxidrome from the anticholinergic toxidrome

271
Q

What is the treatment for sympathomimetic overdose?

A

■ Supportive care
■ cooling measures
■ IV hydration
■ Benzodiazepines: For agitation, hyperthermia, tachycardia, seizures, muscular
rigidity
■ Sodium bicarbonate: For wide complex dysrhythmias

AVOID BETA BLOCKERS
- leads to unopposed alpha receptor stimulation

ITE '23 (20 decks)

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