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Toxicology Flashcards

1
Q

Assessing a Patient when suspicious for o/d

A

First Steps – ABCD3EF

  • ABCs
    • Intubation and mechanical ventilation as needed
  • D3
    • Disability assessment - neurologic exam/pupils/level of consciousness
    • Empiric Drug therapy – oxygen, dextrose, naloxone (AMS)
    • Initial Decontamination – ocular/dermal/GI decontamination
  • E.F.
    • E – ECG
    • F – Fever/Temperature
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2
Q

Toxicokinetics & Toxicodynamics

A
  • Evaluate ADME
  • Evaluate effects to body by toxic substances
    • Toxic effects may be different from therapeutic action
  • Slowed absorption
    • Formation of poorly soluble concretions in GI tract (Bezoar)
    • Slowed GI motility
    • Toxin-induced hypo-perfusion
  • Decreased protein binding
  • Decreased elimination
    • Saturation of biotransformation pathways
  • Prolonged toxicity due to longer-acting metabolites
  • End organ damage; Is the toxic substance renal/hepatic cleared
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3
Q

GI Decontamination: Activated Charcoal (AC)

A
  • KEY: Decrease absorption and systemic exposure
    • Effect occurs in the GI tract
    • Toxin forms a complex with activated charcoal
  • Indication
    • Toxin known to be absorbed
    • Within 1 hour of ingestion
  • After 1 hr. (Up to 4 hrs.) evaluate if:
    • Prolonged gastric emptying
    • Toxin properties
    • Bezoar formulation
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4
Q

AC Dosing

A
  • Optimal dose based on minimum dose needed to completely absorb toxin – Ideal ratio of charcoal: toxin is ratio of 10:1
  • Flat Dosing
    • Adolescents/Adults 50-100 grams (Will absorb 5-10 grams of toxin)
    • Children 0.5-1 gram/kg
  • When calculation of 10:1 ratio exceeds flat dosing, consider gastric emptying or MDAC
  • Gritty texture, sticky and cakes
  • Ideal to mix with water/juice
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5
Q

AC Contraindications and AC Adverse Effects

A
  • Clinically meaningful amount of toxin not absorbed
  • Absent airway protective reflexes or not intubated
  • GI perforation likely (caustic ingestions)
  • Increased risk and severity of aspiration (hydrocarbons with high aspiration potential)
  • Endoscopy anticipated (caustics)

AE:

  • GI effects
  • Constipation, nausea, fullness
  • Vomiting ~20%
    • Some studies show no difference compared to control group
    • Greater when administered with sorbitol or via NG tube
    • Greater after rapid ingestion of larger doses
  • Pulmonary Aspiratory
    • Misplaced tubed - aspiration of gastric contents and instillation into lungs
    • Lower incidence in intubated patient
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6
Q

Multi-Dose Activated Charcoal (MDAC)

A

Sequential doses of AC; Same contraindications/adverse effects

KEY:

  • Prevent ongoing absorption if toxin persists in GI tract
  • Enhance elimination in post-absorptive phase – interrupt enterohepatic recirculation of medications
  • Dosing regimens are individualized
    • 0.5 grams/kg or 25-50 grams Q4-6 hours up to 12-24 hours
  • Benefits
    • Life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine, salicylates or theophylline
    • Enterohepatic or enteroenteric recirculation and adsorbed by AC
    • Toxin persists in GI tract
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7
Q

Gastric Lavage

A
  • KEY: Remove toxic potential before absorption
  • Not indicated in all situations – evaluate risks & benefits
    • Utilized with potentially life threatening amount
    • Especially if within 60 minutes of ingestion
  • Place orogastric tube
    • Wash out gastric contents through repetitive instillation and withdrawal of fluid

Lavage Not Indicated

  • Limited toxicity at almost any dose of toxin
  • Well adsorbed by activated charcoal
    • Amount ingested not expected to exceed adsorptive capacity
  • Significant spontaneous emesis has occurred
  • Patient presents many hours post-ingestion with minimal signs/symptoms of poisoning
  • Highly efficient antidote available

Lavage Contraindications​

  • Respiratory
    • No airway protective reflexes
    • Not intubated
    • High aspiration potential in absence of intubation
  • GI
    • Patient at risk of hemorrhage or GI perforation
  • Toxin
    • Alkaline caustic agent
    • Foreign body
    • Too large to fit into lavage tube

Lavage Adverse Effects

  • Injury to esophagus and stomach
  • Electrolyte imbalances
    • Significant decreases in calcium and magnesium
    • Severe hypernatremia
  • Respiratory failure
  • Aspiration pneumonitis
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8
Q

Whole-Bowel Irrigation (WBI)

A

Purging GI tract to achieve gut clearance and prevent further absorption

  • Oral or NG administration of PEG solution
    • 1-2 Liters/hour
    • Continue until rectal discharge clear
  • Indications
    • Toxic ingestion of SR tablets and metals
    • Ingestion of illicit drug packets (drug smuggler)
    • Toxin has slow absorptive phase
    • Not absorbed by activated charcoal
    • Other methods are not safe or beneficial

Irrigation Contraindications:

  • Inadequate airway protection
  • GI tract not intact
    • Significant GI bleed
    • Obstruction
  • Uncontrolled vomiting
  • Signs of leakage from cocaine packets (surgical removal)
  • Do not administer with activated charcoal
    • Administered AC after irrigation
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9
Q

Syrup of Ipecac

A
  • Not Recommended
    • Was utilized to induced vomiting
    • Contraindicated with caustics and corrosives
    • Contraindicated if no gag, lethargy, comatose, seizing
  • Has not shown to be of benefit
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10
Q

Enhanced Elimination

A
  • Diuresis
    • If toxins eliminated primarily by kidneys
    • Monitor fluids and electrolytes
  • Urine alkalization for weak acids
    • Sodium bicarbonate bolus followed by continuous infusion
    • 1.5 - 2x maintenancerate
    • Complications - Alkalemia, Hypokalemia
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11
Q

Hemodialysis

A
  • Especially if symptoms persist or worsening clinical status
  • Corrects fluid/electrolyte imbalance
  • Enhances removal of some toxic metabolites
    • Molecular weight, water solubility, protein binding, distribution
    • Large Vd – hemodialysis may be ineffective
  • If dialyzable
    • Effective: Salicylates, ethanol, phenobarbital, lithium, VPA, phenytoin
    • Ineffective: Amphetamines, antidepressants, antipsychotic agents • CCB, digoxin
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12
Q

Supportive Therapy in OD

A
  • Agitation
    • Short acting benzodiazepines
    • Antipsychotic agent (haloperidol or olanzapine)
  • Delirium
    • Agitation with abnormal vital signs: benzodiazepines
    • Normal vital signs: haloperidol
  • Seizures: short acting IV benzodiazepines
  • Hyperthermia: external cooling; control agitation
  • Hypotension: fluid bolus, inotropic agents
  • Bradycardia: atropine
  • Manage cardiovascular complications
  • Rhabdomyolysis – Adequate hydration to maintain urine output
  • Hemodialysis may be required
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13
Q

Antidotes

A
  • Acetaminophen - N-acetylcysteine
  • Benzos - Flumazenil
  • B-Adrenergic antagonists (B-blockers) - Glucagon
  • CCBs - Calcium, High-dose insulin euglycemia, IV lipid
  • Coumadin - Vit K
  • Cyanide - Hydroxocobalamin, sodium nitrate and sodium thiosulfate
  • Digoxin - Digoxin immune Fab
  • Ethylene glycol - fomepizole, ethanol
  • Iron - deferoxamine
  • Isoniazid - pyridoxine
  • Lead - British anti-Lewisite
  • Organophosphorus insecticides and nerve agents - atropine, octreotide
  • Tricyclic antidepressants - Sodium bicarb, IV lipid
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14
Q

Acetaminophen Metabolism

A
  • ~95% hepatic conjugation to inactive metabolites eliminated in urine
    • Glucuronidation and Sulfation
  • ~5% oxidized to reactive toxic intermediates
    • CYP2E1 and CPY3A4
    • Forms end product NAPQI (N-acetyl- p-benzoquinoneimine)
  • Glutathione (GSH) quickly combines with NAPQI via GSH Conjugation
    • Complex converted to nontoxic conjugate eliminated in urine
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15
Q

Tylenol: Assessing Risk of Toxicity

A

Acute vs. Chronic

  • 7.5 g or 150 mg/kg – lowest acute dose capable of causing toxicity
  • 12 grams or 200 mg/kg – will cause hepatotoxicity

PK

  • Time to peak may be delayed by food and co-ingestion of opioids or anticholinergics
    • ER formulations has a delayed absorption; ~4 hours
  • Assess laboratory findings - LFTs, PT/INR, glucose, SCr
  • Assess signs and symptoms; Patient history
    • How much (how many, what strength); How long ago;
  • Assess APAP serum level compared to time of ingestion
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16
Q

Rumack-Matthew nomogram

A
  • Define earliest possible ingestion time
  • Patients with levels below treatment line do not require further evaluation or treatment
  • Early levels before 4 hours only rule out APAP ingestion
    • Repeat if level is detectable
  • “Nomogram Crossing”
    • Occurs more commonly with extended release
  • IV Acetaminophen -New lower line at 50 mcg/mL ??
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17
Q

APAP OD: Special Situations

A

IF ingestion time is > 24 hours

  • Assess APAP level and AST concentration; if AST high, then treat

Chronic Overdose

  • Assess AST/ALT levels; APAP level
  • Assess risk factors
    • S/S;
    • Chronic INH ingestion; malnutrition, anorexia
    • Risk of increased NAPQI formation or decreased GSH stores
  • Drug Interactions (APAP is metabolized to NAPQI by CYP2E1)
    • Inducer will increase risk of hepatotoxicity
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18
Q

APAP OD: Management

A
  • Gastrointestinal decontamination
    • Generally not recommendation due to very rapid GI absorption
  • Supportive care
    • Control N/V
    • Manage hepatic injury
      • Hypoglycemia
      • Coagulopathy
  • Manage renal injury
  • Administer Antidote N-acetylcysteine
    • Nearly 100% effective if started within 6-8 hours post ingestion
      • Before glutathione stores are depleted to ~30% of normal
    • NAC1 augments sulfation
    • NAC2 is a GSH precursor
    • NAC3 is a GSH substitute
    • NAC4 improves multi-organ function during hepatic failure and may limit extent of hepatocyte injurt
19
Q

NAC Routes of Administration

A
  • Equally efficacious IV or PO
  • Consider rate of adverse events
    • Mild reactions overall
    • n/v 20% PO; 7%IV
    • Anaphylactic reactions ~14-18% IV
  • Cost - Drug versus Hospital stay
  • IV preferred if:
    • Fulminant hepatic failure
    • Inability to tolerate PO (AMS)
    • APAP poisoning in pregnancy??
20
Q

NAC Dosing

A

Oral (Mucomyst):

  • 140 mg/kg loading dose
  • 70mg/kg q4 x 17 doses
  • Total 1330 mg/kg in 72 hours
  • Diluted and mix with juice or soda 3:1 ratio

Intravenous (Acetadote):

  • 150 mg/kg (max 15 grams) infused over 1 hour
  • 50 mg/kg (max 5 grams) infused over 4 hours
  • 100 mg/kg (max 10 grams) infused over 16 hours
  • Total 300 mg/kg in 21 hours
21
Q

Salicylate OD

A

Salicylate pharmacokinetics

  • Available in a variety of OTC products
  • Rapidly absorbed from stomach
  • T1⁄2 for aspirin and salicylate metabolite
    • Antiplatelet doses ~2-3 hours
    • Anti-inflammatory doses ~12 hours
  • • Hepatic transformation and Renal elimination
  • Protein binding ~90% (decreased in overdose)

Altered PK in overdose​

  • Decrease in protein binding due to saturated binding sites
  • Longer half-life
  • Elimination pathways become saturated = increase in tissue/brain concentrations
22
Q

Salicylate OD Clinical Manifestations

A

Clinical Manifestations

  • Early s/s:
    • GI irritation/N/V
    • Direct central respiratory stimulation leads to hyperventilation and respiratory alkalosis
  • Develops into mixed acid-base disturbance with respiratory alkalosis plus metabolic acidosis — Severe if respiratory acidosis develops
  • Neurological most visible and concerning
    • Confusion, lethargy, cerebral edema, coma
    • Difference in CSF and serum glucose; CSF decreased by 33%
23
Q

Salicylate Analysis

A
  • Determining Serum Levels via Trinder assay
  • Watch your units - US mg/dL (mg/L and mcg/mL)
    • Therapeutic level 10-30 mg/dL
    • Toxic levels > 30 mg/dL
  • Correlation between levels and toxicity variable and dependent on pH and could be misleading
    • Acidemia = more salicylate has crossed into CSF/tissues
24
Q

Salicylate OD Management

A
  • GI Decontamination
    • AC reduces absorption ~50-80%, sooner better
    • 10:1 ration of AC to ingested salicylates
    • In massive ingestion, multiple doses (MDAC) to achieve desired ratio – efficacy debatable
  • Fluids
    • Need only to correct for fluid and electrolyte disturbances
    • BUT no forced diuresis
      • Increasing diuresis may lead to hyperventilation, vomiting, hyper-metabolic state
  • Enhance Elimination with Serum and Urine Alkalinization
  • Sodium Bicarbonate IV
    • IV Bolus, followed by continuous infusion
    • 132 mEq/L D5W at 1.5 – 2x maintenance rate
    • Goal: maintain urine pH at 7.5-8
    • Monitor
      • Hypokalemia and hypocalcemia
    • Supportive care
    • Hemodialysis is an option
25
Q

Salicylate OD: When should HD be considered..

A
  • Kidney failure
  • Acute Respiratory Distress Syndrome
  • Persistent CNS disturbances
  • Progressive deterioration in vital signs
  • Severe acid–base or electrolyte imbalance despite treatment
  • Hepatic compromise with coagulopathy
  • Salicylate concentration (acute) >90 mg/dL
  • Chronic poisoning in those with concerning symptoms regardless of salicylate concentrations
26
Q

NSAID OD

A

NSAIDs

  • Highly protein bound
  • Plasma t1⁄2 range from 1-2 hours to 50-60 hours
  • Undergo hepatic metabolism w/ renal excretion of metabolites

Overdose symptoms seen within 4 hours

  • Initial – mild and mainly GI (N/V/pain) and CNS (drowsiness, headache, tinnitus, diplopia, dizziness)
  • Moderate/Severe – coma, seizures, CNS depression, metabolic acidosis, rhabdomyolysis, dysrhythmias, hypotension, electrolyte abnormalities, AKI; severe leads to multi-organ failure

Management:

  • Supportive Care
    • Children with > 400 mg/kg are high risk of toxicity
  • GI Decontamination
    • Activated Charcoal should be considered first
    • Massive OD - Gastric lavage followed by AC
    • SR Formulations – Multiple doses of AC
  • IV fluids, airway management, EKG
    • Hypotension, electrolyte disturbances, conduction disturbances, unresponsive patients
  • Dialysis for acid-base correction
27
Q

Anticholinergic Agents OD

A
  • Large number of medications possess anticholinergic properties
  • Inhibit Acetylcholine (ACh) at muscarinic receptors producing the classic anticholinergic syndrome:
    • “Red as a beet” – flushed skin
    • “Hot as a hare” – hyperthermia
    • “Dry as a bone” – dry mucous membranes
    • “Blind as a bat” – blurry vision
    • “Mad as a hatter” – confusion, delirium

Management

  • Supportive care
    • Agitation – Benzodiazepines; Antipsychotics

Antidote for Anticholinergic effects – Physostigmine

  • Note: Do not use in TCA overdose due to exacerbation of cardiotoxicity
  • Primarily used in medications that have anti-muscarinic properties (scopolamine, benztropine)
  • MOA – Inhibits destruction of ACh by acetylcholinesterase
28
Q

CALCIUM CHANNEL BLOCKERS and Β-BLOCKERS overdose

A

Hypotension and Bradycardia

Management

  • GI Decontamination
  • Especially if SR formulation
  • Contraindications?
  • Symptomatic or asymptomatic?

Activated Charcoal

  • MDAC – efficacy in continuously absorbing SR formulation

Supportive Care

  • EKG monitoring and continuous cardiac monitoring
  • Intubation if necessary
  • Focus on maintaining/improving cardiac output and peripheral vascular tone
29
Q

Ca-Channel Blockers and Beta-Blocker overdose management

A

Step#1

  • Fluid boluses
    • Caution with aggressive fluid resuscitation
  • Atropine
    • Treatment of symptomatic bradycardia
    • Improves heart rate and cardiac output
    • Risks versus benefits??
      • Decreases GI motility
  • Calcium
    • Increases extracellular calcium
    • Improves blood pressure
    • Caution with extravasation
  • Glucagon
    • Functions as “pure” β1 agonist with no peripheral vasodilatory effects
      • Increases heart rate, contractility, and blood pressure
    • Drug of choice for β-blocker overdose
    • Dosing - IV bolus, followed by continuous infusion

Step #2

  • If non-responsive to Step 1 – move onto step 2
    • Hyperinsulinemia-euglycemia therapy
    • 20% IVFE
30
Q

Insulin-Euglycemia Therapy/High-dose insulin euglycemia (HIE)

A
  • Myocardial tissue becomes carbohydrate dependent for metabolic needs
  • Myocardium becomes insulin resistant
  • Improved contractility
    • Calcium mediated insulin secretion from β-islet cells in pancreas inhibited by CCB
  • Insulin bolus (w/dextrose unless glucose > 300 mg/dL)
    • Followed by Insulin infusion
  • Monitor glucose q30 minutes x 4 hours
  • What else should be monitored?
31
Q

Lipid Emulsion 20%

A
  • Activates ion channels including calcium
  • Enhances intracellular metabolism
  • Acts as lipid sink to sequester lipid soluble drugs
    • Lowers free serum concentrations
    • **Highly lipophilic drugs benefit more
  • Especially effective for CCB and propranolol
32
Q

Antipsychotics

A
  • Mild intoxication
    • Sedation, hypotension, miosis
  • Severe intoxication
    • Agitation & delirium, seizures, cardiac arrhythmias, respiratory arrest, and coma
    • Dystonias and pseudoparkinsonism may occur
  • Treatment: supportive
    • Gastric lavage, activated charcoal
    • Hypotension; Seizures
    • CV: Sodium bicarbonate
33
Q

Neuroleptic Malignant Syndrome

A
  • Life Threatening Emergency
  • Cardinal symptoms
    • T >38 (100.4), altered level of consciousness, rigidity, autonomic dysfunction (tachycardia, labile BP, diaphoresis, tachypnea, or urinary/fecal incontinence)
  • Risk factors: dehydration, physical exhaustion, organic mental disease
  • Treatment: supportive care, dantrolene
    • Time to presentation – NMS develops more gradually compared to Serotonin Syndrome which has a rapid onset
34
Q

TCA OD

A
  • Class 1A antiarrhythmic agents – lethal arrhythmias
  • Treatment:
    • Sodium bicarbonate to displace TCA from cardiac Na++ channels
    • Torsade’s – Magnesium Sulfate IV
    • Must correct acidosis and hypoxia; hypotension
    • CNS toxicity - Seizures
35
Q

Carbon Monoxide (CO)

A
  • Mechanism of toxicity:
    • Binds to hemoglobin leading to carboxyhemoglobin (COHb)
    • COHb CANNOT transport oxygen leads to decrease in oxygen delivery to cells
  • Initially - Headache, dizziness, nausea, confusion
  • Later – Tachycardia, tachypnea, myocardia ischemia
  • Clinical Pearl: Many cases of CO toxicity arise in the winter time and are misdiagnosed as influenza due to atypical initial signs and symptoms **Evaluate COHb level
    • Normal Level (non-smoker): 0 – 5 %; (smoker): 6 – 10%

Management

  • 100% Oxygen!
    • Administration of O2 will antagonize COHb
    • Decreases half-life of CO from ~220 min at room air to ~80 min
  • Hyperbaric oxygen (Hyperbaric Chamber)
    • Treatment of choice in significant CO exposures
    • Administration of 100% O2 under increased pressure
    • Decreases the half-life of CO to ~ 40 min

• In NY - Hyperbaric Oxygen (HBO) Program at NewYork-Presbyterian Hospital

36
Q

Chelating Agents

A

Edetate calcium disodium (Calcium EDTA)

  • Indication: Lead poisoning

Dimercaprol

  • Indication: Severe lead, arsenic, and mercury toxicity

Succimer (Chemet®)

  • Indication: Lead, mercury, and arsenic exposures
37
Q

Drug abuse: Dopamine’s Role in Reinforcement

A
  • Prime target of addictive drugs: Dopaminergic Mesolimbic Tract
    • Function: Arousal, memory, stimulus processing, motivational behavior
    • Central role in Reward Processing – increase the level of dopamine reinforcement and risk of psychosis
  • Prime target of non-addictive drugs: Cortical and Thalamic circuits
    • Examples: LSD, PCP and ketamine
    • Substances that alter perception without feelings of reward/euphoria (feeding detached from reality)
    • Can cause anxiety, memory loss, impaired motor function
38
Q

Amphetamines “Club Drug”

A
  • Smoked, injected, or swallowed
    • Methylene-dioxymethamphetamine (MDMA) – Ecstasy; 3,4 Methylenedioxyamphetamine(MDA, love drug), Methamphetamine (speed, uppers); Cathinone (Methcathinone, MDPV, Mephedrone) - Bath Salts
  • Lipophilic
  • Hepatic versus renal
    • Dependent on compound
    • CYP1A2, CYP2D6*, and CYP3A4
    • Extensive renal elimination

PK

  • Induction of catecholamine release
    • Spills dopamine, norepinephrine, serotonin into synapse
    • Stimulates α-adrenergic receptors, β-adrenergic receptors, dopamine, and serotonin
  • Serotonin – primarily responsible for hallucinogenic and illusion properties
  • Norepinephrine – primarily responsible for vasoconstriction and increased cardiac activity
  • Chronic administration alters catecholamine transporter functions, depletes catecholamine and produces irreversible destructions of neurons
39
Q

Inhalants

A
  • Nitrates, ketones, hydrocarbons
    • “sniffed”: inhale from open container
      • “huffed”: inhale cloth soaked with inhalant
      • “bagged”: inhale bag filled with inhalant
  • Highly lipophilic, stimulate GABAA
  • Initially.. Euphoria, hallucinations (visual and auditory) • Headaches, dizziness
  • Toxicity
    • Slurred speech, confusion, tremor, weakness
    • Seizures, coma, respiratory depression
    • Dysrhythmias (poor prognosis)
    • Hepatotoxicity, renal toxicity with electrolyte abnormalities
  • Acute cardiotoxicity “sudden sniffing death”
    • Inhalant “sensitizes the myocardium”
  • Long term toxicity: white matter lesions seen in CNS
  • Treatment of overdose – Supportive therapy
40
Q

Cannabinoids

A

Cannabinoids

  • Exogenous cannabinoids
  • Δ9-tetrahydrocannabinol (THC) – Principle psychoactive
  • Central and Peripheral Cannabinoid receptors (CB1 and CB2)
    • Inhibit adenylyl cyclase and stimulate potassium channel conductance
  • Affect acetylcholine, noradrenaline, dopamine
  • CB1 – affects regulation of cognition, memory, motor activities, nociception, N/V

Chronic exposure leads to dependence

  • Withdrawal - Mild and short
    • Restlessness, irritability, insomnia, nausea
    • Supportive therapy
  • Cannabinoid Hyperemesis Syndrome
    • Abdominal discomfort, nausea, hyperemesis • Refractory to opioids and anti-emetics
    • Hallmark of Syndrome:
      • Immediate relief of symptoms with hot showers/baths • Leads to compulsive hot showers/baths
41
Q

Nicotine

A
  • Mimics effects of acetylcholine release
  • Binds to nicotinic receptor (nAChR)
    • Located in the brain, spinal cord, autonomic ganglia, adrenal medulla, neuromuscular junctions
    • nAChR expressed on Dopamine neuron – dopamine released
  • Clinical effects are dose-dependent
  • Treatment of addiction
    • Short-acting medication “relievers” (nicotine nasal spray, inhaler)
    • Long-acting medication “controllers”
      • Varenicline (Chantix)
        • Partial nicotine receptor agonist
        • Suicidal ideation is very concerning
        • SE: N/V/C, vivid dreams, headache, insomnia
      • Bupropion (under brand name Zyban)
        • Lowers seizure threshold** caution if history of seizures

Nicotine Replacement Therapy (NRT)

  • Patch
    • Apply to clean, dry, relatively hairless part; change locations daily • AE: Skin irritation, erythema, burning, insomnia
  • Gum/Lozenge can be added to patch
    • Do not eat or drink (except water) 15 min before or while using
    • AE: Nausea or heartburn if swallowed
  • Gum Directions
    • Chew until peppery taste (~15 chews), park gum between cheek & gum; when taste diminishes, resume chewing until peppery taste again, then park gum in different area of mouth
  • Lozenge Directions
    • Rotate throughout mouth until dissolved; Do not chew or swallow
42
Q

Binge Drinking

A
  • Original Definition - 5 drinks in 2 hours (based on men)
  • National Institute on Alcohol Abuse and Alcoholism (NIAAA) defined binge drinking as pattern of drinking that brings person’s blood alcohol concentration (BAC) to ≥ 0.08%
  • Youth likely to reach higher BAC with 5 drinks in 2-hours
    • Girls 9-17 yo & Boys 9-13 yo ≥3 drinks
    • Boys 14-15 yo ≥4 drinks
    • Boys 16-17 yo ≥5 drinks
43
Q

Alcohol BAC Levels

A
  • BAC of 50 to 150 mg/dL – Intoxication
    • Consequence of alcohol entering bloodstream faster than it can be metabolized by liver
    • Initial euphoria followed by incoordination, imbalance, ataxia, sleepiness, loss of social inhibitions, depression, and hostility
  • BAC > 150 mg/dL – More depressant symptoms
    • Lethargy, bradycardia, hypotension, and respiratory depression
  • BAC > 450 mg/dL – Alcohol poisoning
    • Stupor, coma, and death by respiratory depression with respiratory acidosis and hypotension
  • Seizures - More common to occur in children with hypoglycemia

Management

  • Supportive Care
    • Benzodiazepine +/- haloperidol
    • Intubation
  • GI decontamination
    • Recent ingestion, delayed absorption, concomitant ingestions
  • Hypoglycemia
  • Evaluate need for therapy (inpatient or outpatient)
44
Q

Benzodiazepine Reversal

A
  • Enhance GABAA receptor activity
  • Dependence is common; addiction is rare
  • Withdrawal (symptoms taper within 1-2 weeks)
    • Occurs within days of discontinuation (depends on T1/2)
    • Irritability, insomnia, phono- or photo-phobia, seizures
  • Reversal of benzodiazepines: Flumazenil
    • Shorter t1⁄2 compared to BZD – requires multiple doses
    • Caution w/inducing abstinence/withdrawal syndrome

ped pharm (13 decks)

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