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EM - Exam 3 > Toxicology Emergencies > Flashcards

Toxicology Emergencies Flashcards

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1
Q

Define addiction

A

Compulsive engagement in rewarding stimuli (despite adverse consequences)

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2
Q

Define dependence

A

Adaptive physiologic state due to recurrent exposure to a substance (resulting in withdrawal when ceased)

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3
Q

Describe heroin and its common street names

A
  • Derived from the opium poppy
  • First made in 1874
  • H, smack, boy, horse, brown, black, tar
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4
Q

Pathophys of heroin use

A
  • Enters bloodstream
  • Converted to morphine by enzymes
  • Morphine binds opiate receptors in reward pathway stimulating DA release
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5
Q

Onset and duration of heroin

A
  • Onset seconds to minutes

- Duration 2-6 hrs

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6
Q

Methods of heroin use

A
  • Injecting
  • Smoking
  • Snorting
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7
Q

What is “speedballing”?

A

Simultaneous IV injection of heroin and cocaine

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8
Q

Effects of heroin use

A
  • CNS and resp depression
  • Constricted (pinpoint) pupils
  • Nausea
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9
Q

Treatment of heroin abuse/OD

A
  • Acute OD requires Narcan (Naloxone)
  • Observation
  • Abscesses may need draining
  • Consider endocarditis
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10
Q

What is naloxone (Narcan)?

A

Competitive opioid antagonist (blocking all opioid receptors)

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11
Q

Formulations of Naloxone

A

IV, IM, SC or ET routes

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12
Q

Usual starting dose of Naloxone?

A

0.4 mg

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13
Q

Naloxone duration of action

A

30-60 mins

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14
Q

Caution of Naloxone?

A

May induce vomiting and agitation

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15
Q

Commonly abused prescription opiates:

A

Vicodin
Percocet
Fentanyl

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16
Q

Prescription opiate OD compared to heroin?

A

Slower onset but effects last longer

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17
Q

S/s of opiate withdrawal

A
  • Mildly increased temp
  • Yawning
  • Rhinorrhea
  • Midriasis
  • Vomiting, diarrhea, cramps
  • Myalgias
  • Irritability
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18
Q

Treatment of opiate withdrawal

A
  • Clonidine
  • Dicyclomine (cramps)
  • Loperamide (diarrhea)
  • Hydroxyzine (anxiety/sleep)
  • Ibuprofen (pain)
  • Methadone program (for long term)
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19
Q

Describe cocaine and its common street names

A
  • Naturally derived CNS stimulant extracted/refined from coca plant
  • Crack, freebase, coke, blow, rock, crank
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20
Q

Pathophys of cocaine use

A
  • Binds Na channel, blocks ion conduction within myocardial and nerve cells
  • Inhibits monoamine reuptake systems (resulting in enhanced actions of norepi, epi, DA)
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21
Q

Onset and duration of cocaine

A
  • Onset seconds to mins

- Duration 20-40 mins

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22
Q

Methods of cocaine use

A
  • Snorting (MC)
  • Oral
  • Intranasal
  • IV
  • Smoking
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23
Q

S/s of cocaine use

A
  • Euphoria
  • Paranoia
  • Increased energy, sexual stimulation
  • HTN, tachycardia, coronary vasospasm
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24
Q

EKG effects of cocaine use

A
  • Prolonged QRS, QT, QTc intervals
  • STEMI
  • V tach/fib
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25
Treatment of cocaine use
- Benzos (Lorazepam) - IVF - BP management (nitro, AVOID B blockers due to unopposed alpha-adrenergic activity) - Long term treatment via CBT, support networks
26
Cocaine withdrawal
No true withdrawal - more of a hangover (requires rest/time)
27
When managing BP in cocaine use, what should be avoided?
B Blockers (due to unopposed alpha-adrenergic activity)
28
Describe synthetic marijuana
- Marketed OTC as "incense" or "potpourri" under the names Spice, K2, etc. - Consists of various controlled substances
29
Pathophys of synthetic marijuana
Synthesized compounds bind much more strongly to THC receptors than regular marijuana which can lead to powerful, unpredictable, dangerous effect
30
Onset and duration of synthetic marijuana
- Onset 15-30 mins | - Duration 2-6 hrs
31
S/s of synthetic marijuana use
- Severe agitation, anxiety - Fast HR and higher BP - NV - Muscle spasms, seizures - Intense hallucinations - Suicidal thoughts/actions
32
Synthetic marijuana use is linked to the development of what?
Pneumonia
33
Treatment of synthetic marijuana abuse
Benzos (Lorazepam/Ativan) - may require large doses...wait it out
34
Describe bath salts
- Derivative of khat plant used as a stimulant | - Vanilla Sky, Cloud Nine, Ivory Wave, etc etc
35
Pathophys of bath salts
Acts on monamine neurotransmitters as DA-Norepi reuptake inhibitors (leads to an increase in serotonin and, lesser extent, DA)
36
Methods of bath salts use
- Snorted (MC) - Ingested - Injected - Smoked - Rectal
37
Onset and duration of bath salts
- Onset 30-90 mins | - Duration 2-4 hrs
38
S/s of bath salts use
- "Excited delirium" - Tachy, HTN, chest pains - Paranoia, hallucinations - Rhabdo, renal failure
39
Treatment of bath salts abuse
Benzos (Lorazepam/Ativan) - may require large doses (wait it out)
40
Describe amphetamines and street names
- Began as an OTC bronchodilator - Today used primarily for ADD/ADHD - Street names: crystal meth, speed, crank, ice, glass
41
Pathophys of amphetamines
- Stimulates release of DA and serotonin - Dopamine stores become depleted resulting in depression and need to reuse - Destruction of DA and serotonin brain cells over long term use
42
Methods of amphetamine use
- IV - Smoking - Snorting - Pill abuse (Adderall)
43
Onset and duration of amphetamines
- Onset quick high lasting 5-30 mins | - Duration 6-12 hrs
44
S/s of amphetamines use
- Euphoria, increased activity - Increased BP, RR - Hypertermia, insomnia - Cracked teeth - Sores, skin infections
45
Treatment of amphetamine abuse
- Haloperidol (IM) for agitation - Lorazepam IM/IV for agitation/seizures - Labetalol IV for HTN/tachy
46
Describe CNS depressants and common street names
- Early use as medical anesthetics, ETOH withdrawal | - GHB, Rohypnol, rophie, G, liquid ecstasy, "date rape drug"
47
Pathophys of CNS depressants
Impairs dopaminergic transmission, MOA poorly understood
48
Methods of CNS depressant use
Mostly oral
49
Onset and duration of CNS depressants
- Onset 15-30 mins | - Duration 2-12 hrs (90 mins peak)
50
S/s of CNS depressant use
- Euphoria, decreased inhibitions - Sleepiness/lethargy - Muscle relaxation - Confusion, loss of balance, HA, NV
51
Treatment of CNS depressants abuse
- ABCDEs - SANE (rape) kit and police if suspected - Supportive measures - Physostigmine IV (generally reserved for severe overdose)
52
Describe how activated charcoal is formed
- Wood heated to high temps then oxidized using acid and steam - Produces fine particles that are almost pure carbon - Resulting structure has an enormous surface area
53
How is activated charcoal used medically?
- Acts as a "sponge" to absorb chemicals/meds that are not yet absorbed from GI tract into circulation - Usually given w/Sorbitol which acts as a laxative
54
Activated charcoal is NOT useful for:
- Corrosives/solvents - Iron salts - Lithium - Boric acid - Arsenic - Ethanol
55
When is activated charcoal most effective?
If given within 30-60 mins of ingestion (min use after 3 hrs)
56
Describe gastric lavage and when it is most effective
- Used infrequently | - Most effective if within 30-60 mins of ingestion
57
Indications for gastric lavage
- Removal of toxins in massive OD or highly toxic ingestions | - Dilute/remove corrosive liquids and to empty stomach in preparation for EGD
58
Describe whole bowel irrigation
PEG Lyte given at high flow rates (2 L/h) to force intestinal contents out by sheer volume (until rectal effluent is clear)
59
Indications for whole bowel irrigation
- Large ingestions of Fe, Li, other drugs poorly adsorbed to AC - Large ingestions of SR or EC tablets of valproic acid, theophylline, ASA, verapamil, dilt - Ingestion of FB or drug filled packets in body stuffers/packers
60
Contraindications to whole bowel irrigation
- Ileus or intestinal obstruction - Obtunded - Comatose - Convulsing
61
MC cause of acute liver failure in US?
Acetaminophen overdose
62
Survival rate of acute OD of APAP?
100% if effectively treated within 8 hrs of ingestion
63
Pathophys of APAP use
- Release of cytokines, nitrogen, O2 radicals initiates secondary inflamm response within hepatic parenchyma - Can lead to fulminant liver failure (often irreversible) - Clotting and renal dysfunctions possible
64
Onset of APAP
- Completely absorbed within 2 hrs BUT serum concentrations peak within 4 hours - Liver injury may occur w/in 8-12 hrs - Hepatic necrosis/failure in 3-5 days
65
S/s of APAP abuse
- Asymptomatic | - NV, anorexia, RUQ pain, jaundice, coma
66
Treatment of APAP abuse
- Initiate tx if level meets/exceeds lower line on serum concentration vs. ingestion graph - Activated charcoal w/in 4 hrs - NAC PO or IV (if over 8 hrs since ingestion, pregnant, presents w/hepatic failure)
67
What are some unexpected salicylate sources?
- Pepto Bismol (bismuth subsalicylate) - Alka-Seltzer - Aspercreme - Percodan
68
Pathophys of salicylate use
- Increases resp center sensitivity - Damages hepatocytes - Inhibits platelet organization and AA synthesis
69
Salicylates onset of action
Variable depending on dose/route
70
S/s of salicylates use/abuse
- Tinnitus - NV, fever, lethargy - Diaphoresis, epigastric pain
71
Describe Reyes syndrome
- Hepatic failure w/encephalopathy - A/w ASA use in pediatric viral illness - 30% mortality rate
72
How should salicylate levels be monitored?
- Check 4 hrs after ingestion | - Then every 3 hrs until levels decline
73
Treatment of salicylate overdose
- Activated charcoal - Urinary alkalization to pH of 7.5-8 (D5W mixed w/Na bicarb infused, watch for hypokalemia and hypocalcemia) - Dialysis for severe toxicity
74
Prognosis of salicylate overdose
Depends on serum level 6 hrs after ingestion - Less than 35 mg/L no symptoms - 35 to 70 mg/L mild-mod symptoms - 70 to 100 severe symptoms - Over 120 potentially fatal
75
MC meds with anticholinergic properties
- Tricyclics - Antihistamines - Antispasmodics - Antiparkinsons - Antiemetics - Antipsychotics - Muscle relaxants
76
Pathophys of anticholinergic use
- Blocks muscarinic and nicotinic receptors - CNS blockage results in excitation/agitation - Central blockage causes hypermetabolic states - Peripheral reduces sweat gland function
77
Onset and duration of anticholinergics
- Onset 1-2 hrs - Mild toxicity symptoms resolve in 6 hrs - Severe toxicity or long acting may last 1-2 days
78
S/s of anticholinergic use/abuse
- Red as a beet (flushing) - Dry as a bone (dry skin) - Blind as a bat (mydriasis w/loss of accommodation) - Mad as a hatter (AMS) - Hot as a hare (fever) - Full as a flask (urinary retention)
79
Treatment of anticholinergic OD
- Activated charcoal - Na bicarb for prolonged QRS or arrhythmias - Benzos for agitation/seizures - Physostigmine IV when both peripheral and moderate central toxicity
80
When should physostigmine IV be avoided in anticholinergic OD?
If purely a tricyclic OD (possible asystole)
81
How can serotonin syndrome occur?
- Use of serotonergic agents w/in 2 wks of d/c SSRIs | - Use of MAO inhibitors w/in 5 weeks of d/c fluoxetine
82
Common serotonin syndrome causing meds
- SSRIs - SNRIs - MAOIs - TCAs - Herbal (ginseng, St. John's wort) - Amphetamines, LSD, cocaine
83
Pathophys of serotonin syndrome
Meds cause increased serotonin production and uptake as well as postsynaptic hypersensitivity
84
Onset of serotonin syndrome
50% within 2 hrs, 75% within 24 hrs
85
S/s of serotonin syndrome
- Mental status changes (agitation, confusion, delirium) - Autonomic instability (shivering, midriasis, tachy, HTN, hyperthermia) - Neuromuscular hyperactivity (hyperreflexia, tremor, clonus)
86
Treatment of serotonin syndrome
- Discontinue med (70% resolve within 24 hrs if short acting) - Supportive (cooling and IVF) - Charcoal, benzos - Cyproheptadine (antihistamine) - 25% require intubation
87
Treatment of B blocker overdose?
Glucagon 1-2 mg IV q5min PRN
88
Treatment of CCB overdose?
-Ca gluconate IV or CaCl IV and/or -Glucagon
89
Pathophys of alcohol use
- 90% of ingested alcohol is absorbed by 60 mins - Metabolized in liver at approx 20 mg/dL/h - No specific "alcohol" receptor in body - Effects are CNS depression via desensitization of GABA and NMDA receptors
90
Define alcohol abuse
Continued drinking despite adverse consequences (e.g. legal or social problems)
91
Define alcohol dependence
Alcoholism - Physical cravings and withdrawal symptoms - Need for increasing amounts of alcohol to achieve intoxication
92
Define alcohol withdrawal
Hyperexcitable state due to loss of GABA inhibitory effect and potentiation of NMDA excitatory neurotransmission
93
Describe CAGE
Screening tool for ETOH abuse (1 point for each yes, 2 or more is concerning) - Cut down - Annoyed (by criticism of drinking) - Guilty - Eye opener (drink first thing in AM)
94
S/s of acute mild-mod ETOH intoxication
- Loss of behavior inhibitions - CNS, resp depression - Vasodilation (hypothermia, hypotension) - Tachy - Hypoglycemia - Diminished gag reflex
95
S/s of acute severe ETOH intoxication
- Loss of gross muscle control (ataxia, slurred speech) - Acute pancreatitis/gastritis - Severe myocardial dperession - Lactic acidosis - Pulm edema - Loss of gag reflex
96
Treatment of acute alcohol intoxication
- ABCDEs including gag reflex (sit upright if diminished) - Consider other drug use - Consider underlying depression - Antiemetic (Ondansetron - least sedating) - Observation * IVF do nothing to decrease time to sobriety
97
ETOH withdrawal symptoms
- Tachy, HTN, diaphoresis - Tremors - Insomnia, NV, hallucinations (MC tactile rather than visual) - Psychomotor agitation - Anxiety - Delirium tremens (inattention/disorientation)
98
Treatment of ETOH withdrawal
- Benzos: Lorazepam or Diazepam IV, Chlordiazepoxide PO for hospitalized/home use (long acting and less abuse potential) - Phenobarbital IV (severe cases)
99
How to determine if ETOH withdrawal patients can be managed outpatient?
CIWA-Ar score of less than 8

EM - Exam 3 (6 decks)

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