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1-KWPEM > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What to consider in kids pulled from a housefire??

What signs and symptoms would you see?

A

carbon monoxide, cyanide poisoning
CO: altered mental status +/- cyanosis despite normal pulse ox +/- flu like symptoms if chronic exposure
measure with co-oximeter, treat with 100% non-rebreather, hyperbaric O2
cyanide: headache, dizziness, fast heart rate, shortness of breath, and vomiting. Followed by seizures, slow heart rate, low blood pressure, loss of consciousness, and cardiac arrest

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2
Q

Which medications are potentially life threatening to a 10kg toddler following the ingestion of a single dose?

A 
Sulfonylureas
Propranolol
Clonidine
Calcium channel blockers 
Quinidine (class 1a anti-arrhythmic) 
Disopyramide (antiarrhythmic, Na-channel blocker)
Flecainide (class 1c anti-arrhythmic) 
Chlorpromazine (antipsychotic)
Clozapine (atypical antipsychotic)
Cyclic antidepressants
Hydroxychloroquine (antimalarial) 
Chloroquine (antimalarial)
Buprenorphine (opioid)
Methadone
Diphenoxylate/atropine (lomotil)
Methyl salicylate (wintergreen essential oil)
Camphor (evergreen oil)
Benzocaine (orogel)
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3
Q

What three antidotal drugs should be considered in the resuscitation of the comatose child?

A

oxygen
glucose
naloxone

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4
Q

What basic 5 elements go into the assessment of a toxidrome?

A 
Mental status
Vital signs
pupil size and reactivity
skin color and moisture
bowel sounds
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5
Q

How can you distinguish an anticholinergic toxidrome from a sympathomimetic toxidrome?

A

Both have delirium, psychosis, seizures, increased HR, BP, temperature and pupil size.

In anticholinergic poisoning, the pt has sluggishly reactive pupils, absent bowel sounds and flushed but DRY skin.
Sympathomimetic patients are more likely to be agitated.

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6
Q

What common drugs or intoxicants are poorly absorbed by activated charcoal?

A

ineffective: alcohol, iron, lithium

poorly effective: hydroxycarbons, metals

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7
Q

What are indications for activated charcoal?

A
  • substance known to bind well
  • intact or protected airway (intubated)
  • within 60 minutes of ingestion
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8
Q

List possible indications for whole-bowel irrigation

A 
ingestion of metals, lithium
ingestion of sustained release medications
ingestion of patches
massive overdoses
concretions of pills
body packers or stuffers
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9
Q

Lipid emulsions should be considered (in consultation with a toxicologist) after what ingestions?

A 
bupivacaine
verapamil
beta-blockers
some TCAs
chlorpromazine
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10
Q

What factors predict adequate removal of a poison by hemodialysis?

name 5 examples

A
  • small volume of distribution
  • little protein binding
  • water soluble
  • low molecular weight
  • low endogenous clearance
  • single compartment kinetics

ie: ethylene glycol, lithium, methanol, salicylate, theophylline

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11
Q

Describe the rationale behind urinary alkalinization, what are potential pitfalls?

A

adminitering sodium bicarb or acetate to raise the urine pH to 8 so that renally excreted toxicants, weak acids, are converted to their ionized form within the proximal tubules and not reabsorbed distally (ion trapping). Used in cases like salicylate, phenobarb poisoning, rhabdomyolysis

pitfalls: inhibited in the presence of hypokalemia, associated with pulmonary and cerebral edema, fluid administration to be monitored carefully

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12
Q

Describe the pathophysiology of acetaminophen poisoning

A

After acute overdoses of >150mg/kg/day, the typical metabolism expends all glutathione and results in p450 cytochrome oxidase metabolism and N-acetyl-p-benzoquine. The latter metabolite is toxic to hepatocytes and causes centrilobular liver necrosis.

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13
Q

What are the 4 stages of acetaminophen poisoning?

A

1 (30 minutes-24hrs) often asymptomatic, occasionally nausea, vomiting, diaphoresis, pallor
2 (24-48hrs) nausea, vomiting, RUQ pain, enzymitis
3 (72-96 hrs) fulminant hepatic failure with jaundice, thrombocytopenia, prolonged PTT, hepatic encephalopathy, renal failure, cardiomyopathy
4 resolution

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14
Q

What is the antidote for acetaminophen overdose and how does it work?

A

N-acetylcysteine (NAC)
it replenishes and substitutes for depleted glutathione stores
best benefit if given within 8 hrs of ingestion, IV over 21 hrs
risk of anaphylaxis

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15
Q

What is the approach to acute salicylate poisoning?

When to start advanced care?

A 
Activated charcoal
IV fluids
Urinary alkalization (mild alkalemia will reduce access to the brain)

Avoid intubation or at least mimic resp alkalosis (resp acidemia increases transit to brain)

Hemodialysis if metabolic acidosis, pulmonary edema, severe renal impairment, coma or seizures, liver impairment, level >70mg/dL

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16
Q

How does iron produce toxicity? What does it manifest as?

A

GI stage: vomiting, diarrhea, hypotension (mucosal irritant)

Quiescent stage: stop vomiting and labs worsen

Multiorgan failure with GI hemorrhage and shock (inhibitor of oxidative phosphorylation in the mitochondria)

occasionally 4-6 weeks later gastric scarring with pyloric obstruction

deferoxamine treatment if symptomatic or levels 350-500 can induce hypotension and vin rose pee
no mode of iron excretion (aside from bleeding)

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17
Q

How much iron is toxic? What are the ranges and expected toxicity?

A 
dose ingested: toxicity
20-60mg/kg : mild gastrointestinal symptoms
60-100mg/kg : moderate toxicity
100-200mg/kg : serious toxicity
>200mg/kg : possibly lethal
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18
Q 
How much iron is present in the following commonly available preparations?
ferrous sulphate
ferrous gluconate
ferrous fumarate
Feosol elixir
chewable vitamins
infant liquid vitamins
A 
ferrous fumarate: 105mg (32% 325mg tab)
ferrous succ: 65mg (20% 325mg tab)
ferrous gluconate: 40mg (12% 325mg tab)
Feosol elixir: 44mg/5mL
chewable vitamins: 4-18mg
infant liquid vitamins: 10mg/mL
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19
Q

What is the antidote for iron poisoning?

Risks?

A

Deferoxamine, an iron chelator
5-15mg/kg/hr

associated with pulmonary fibrosis and ARDS

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20
Q

List the major toxicities of cyclic antidepressants

A
  • dysrhythmia (sodium channel blockers in cardiac conduction system)
  • seizures
  • alpha-1 adrenergic blockade
  • inhibition of norepinephrine reuptake
  • anticholinergic toxicity
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21
Q

What electrocardiographic findings correlate wtih potential toxicity from cyclic antidepressants?

A

QRS complex > 0.1 seconds
prolonged QTc for age
R wave height greater than 3 mm for age

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22
Q

What treatment to consider for ventricular dysrhythmia with prolonged QRS interval?

A

consider drug-induced dysrhythmias and give sodium bicarbonate! it has been shown to narrow the QRS and improve function
many agents that cause v-tach in overdose block the fast sodium channels

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23
Q

PALS Brady TRT:

A

atropine, ephinephrine, pacing

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24
Q

What ingestions can cause a brady-dysrhythmia and how to treat?

A

beta blockers
calcium channel blockers
digitalis-containing compounds
clonidine

treat as per PALS: atropine, ephinephrine, pacing
beta blockers -> glucagon, calcium, insulin, lipid emulsions
calcium channel blockers -> calcium, insulin/glucose, lipids
digitalis-containing compounds -> digoxin-specific Fab

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25
Q

How do you treat poison-induced seizures?

Name two special considerations in specific poisoning of cyclic antidepressants and isoniazid

A

Benzodiazepines 1st line
Barbituates (phenobarbital) 2nd line

in cyclic antidepressant overdose DO NOT give IV phenytoin as cardiovascular effects may be complicated

in isoniazid overdose, they need PYRIDOXINE

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26
Q

Describe the findings in a clonidine overdose

A 
miosis
coma
apnea
bradycardia
hypotension
... can mimic opioid ingestion, however clonidine kids often transiently respond to stimulation
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27
Q

Hallucinations or psychosis are prominent in which drugs of abuse?

A
  • anticholinergics (antihistamines, Jimsonweed)
  • dissociatives (PCP, ketamine, dextromethorphan)
  • hallucinogens (LSD, psilocybin, mescaline)
  • sympathomimetics (amphetamines, cocaine, MDMA, bath salts, synthetic cannabinoids)
  • withdrawal from ethanol or sedative-hypnotics
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28
Q

Why should neuroleptics be cautiously used in drug-induced agitation?

A

they lower the seizure threshold, may compound cardiovascular toxicity, may limit ability to dissipate heat

use benzos benzos benzos

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29
Q

Name 7 hyperthermic syndromes in toxicology

A

1) sympathomimetic
2) anticholinergic
3) neuroleptic malignant syndrome
4) malignant hyperthermia
5) serotonin syndrome
6) uncoupling oxidative phosphorylation (salicylate)
7) acute withdrawal

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30
Q

What findings characterize serotonin syndrome?

A

autonomic hyperactivity
increased neuromuscular tone (LEs especially)
hyperreflexia
CNS depression

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31
Q

What are bath salts?

A

synthetic canthiones, related to khat
has similar features to amphetamine overdose
notable for prolonged agitation, aggressive and violent behaviour, hallucinations, paranoia, seizures

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32
Q

How is the osmolar gap calculated?

What is normal

A

osmolar gap=
measured osmolality - calculated osmolality

calculated osmolality= 2(Na) + BUN + glucose

Normal gap -7 to 10 mOsm

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33
Q

List causes of a large osmolar gap

A 
acetone
ethanol
glycols
isopropanol
magnesium
mannitol
methanol
renal failure
severe ketoacidemia
severe lactic acidemia
34
Q

What are symptoms of TCA overdose?
What is the treatment?
What should you NEVER give?

A

Present with altered mental status, anticholinergic toxicity, seizures, wide-complex tachycardias (QRS >100msec).

Treat with NaHCO3, secure airway, activated charcoal if <2hrs.

Do not give:

  • procainamide (worsens cardiac delay)
  • physostigmine (increases seizures)
  • dopamine (ass’ w/ vent dysrhythmias)
35
Q

What is the antidote of choice for beta-blocker toxicity?

A

Glucagon

36
Q

How is the osmolar gap calculated?

What is normal?

A

2{Na}+BUN+glucose

-7 to 10 mOsm

37
Q

List potential causes of an osmolar gap

A
  • acetone
  • ethanol
  • glycols
  • isopropanolol
  • magnesium
  • mannitol
  • methanol
  • renal failure
  • severe ketoacidemia
  • severe lactic acidemia
38
Q

How is alcohol metabolized?

A

According to zero order kinetics, typically it decreases by 15mg/dL/hr

39
Q

What are the toxic metabolites of ethylene glycol and methanol?
What tissues do they damage?
How to treat

A

methanol -> formic acid, toxic to the retina
ethylene glycol -> glycolic and oxalic acids, toxic to the kidneys

alcohol dehydrogenase is responsible for the dangerous transformation, therefore keep it busy with ethanol or fomepizole
adjunctive treatments are folic acid for formic acid
pyridoxine and thiamine for glycolic acids

40
Q

What characteristics of hydrocarbon ingestion make them prone to aspiration?
What’s the clinical presentation?

A
  • low viscosity
  • low surface tension
  • high volatility

Children may cough, gag or sputter at the time. Gradually pneumonitis may develop, usually within 6hrs and 98% within 24hrs.

41
Q

Which hydrocarbons are notable for systemic toxicity?

A 
CHAMPs
Camphor
Halogenated hydrocarbons (carbon tetrachloride, tricholoethane)
Aromatic hydrocarbons (benzene, toluene)
Metal-containing hydrocarbons
Pesticide-containing hydrocarbons

CNS depression, seizures, hepatotoxicity, nephrotoxicity, bone marrow toxicity

42
Q

What are the clinical manifestations of organophosphate or carbamate insecticide poisoning?

A

1) Muscarinic effects (pre&post ganglionic parasympathomimetic)
DUMBELS or SLUDGE with killer B’s
2) Nicotinic effects (preganglionic sympathomimetic)
tachycardia
3) Nicotinic effects (neuromuscular endplate)
muscle fasciculations and weakness
4) CNS system effects
depressed consciousness and seizures

DUMBELS: diarrhea, diaphoresis, urination, myosis, bradycardia and bronchorrhea, lacrimations, salivation
SLUDGE B’s: salivation, lacrimation, urination, diarrhea, GI cramping, emesis, bronchorrhea, bradycardia, bronchospasm

43
Q

What is the treatment for organophosphate or carbamate poisoning?

A

Atropine; repeat dose every 5 minutes with doubling (targets muscarinic effects) END POINT OF THERAPY IS THE DRYING OF SECRETIONS **PULMONARY

Pralidoxime (2-PAM) for organophosphates only, dislodges the aged acetylcholine esterase inhibitor (it regenerates active acetylcholinesterases)

Benzodiazepine

44
Q

What toxins would you consider for hemodialysis?

A

alcohols
salicylates
theophylline
lithium

NO digoxing, NO TCAs (large volume of distribution)

45
Q

How do you calculate an anion gap? What is the normal range?

A

AG= [Na] - [Cl] - [HCO3]

normally <11

46
Q

What is the antidote for acetaminophen

A

NAC

47
Q

What is the antidote for aspirin

A

NaHCO3 & hemodialysis

48
Q

What is the antidote for carbamate

A

atropine and diazepam

not pralidoxime

49
Q

What is the antidote for warfarin

A

vitK FFP

50
Q

What is the antidote for hydrofluoric acid

A

Calcium, magnesium

51
Q

What is the antidote for isoniazid

A

pyridoxine

52
Q

What is the antidote for TCAs

A

NaHCO3

53
Q

What is the antidote for CO

A

oxygen

hyperbaric oxygen

54
Q

What is the antidote for beta blockers

A

glucagon, calcium, insulin, lipid emulsions

55
Q

What is the antidote for calcium channel blockers

A

glucagon, insulin, calcium, intralipid

56
Q

What is the antidote for heavy metals

A

chelators (BAL, EDTA)

57
Q

What is the antidote for iron

A

Defuroximine

58
Q

What is the antidote for cyanide

A

hydroxycobalamine

59
Q

How can you differentiate bradycardic intoxications from digoxin, clonidine, beta-blockers and calcium channel blockers ?

A

digoxin: hyperkalemia, arrhythmias in atria and ventricle, AV block, give Fab fragments
clonidine: looks like opioid with coma, pinpoint, resp depression. Supportive care

beta-blockers: hypoglycemia, treat with IVF, pressors, glucagon, calcium, insulin… ECMO

calcium-channel blockers: inhibits insulin release therefore hyperglycemia… ECMO

60
Q

What is the suffix for sulfonylureas?
What is the mechanism of action?
What is the antidote in intoxications?

A

-ide, like glipizide
increases insulin release from the pancreas
Rx Octreotide (somatostatin analogue) and 2nd line glucagon

61
Q

What is the differential diagnosis for a wide osmolar gap?

A

(ShARP)
¤ Sugar (mannitol,sorbitol)
¤ Alcohols(Ethanol, methanol, ethylene glycol, isopropyl)
¤ Renal Failure
¤ Pseudo-hyponatremia (hyperlipidemia, hyperproteinemia)

62
Q

Name drugs that are readily removed by dialysis

A 
STUMBLED
¤  Salicylates
¤  Theophylline/Caffeine
¤  Uremia
¤  Methanol
¤  Barbiturates
¤  Lithium
¤  Ethylene Glycol
¤  Depakote (Valproic Acid)
63
Q

Name indications for hyperbaric oxygen therapy in carbon monoxide poisoning

A

̈ Neuro symptoms: Syncope, Coma, Seizure, Altered Mental Status/Confusion
̈ Acidosis
̈ COHgB >25%
̈ COHgB>20% in pregnancy

64
Q

What are indications for urine drug screening?

A 
No absolute indications, only relative indications 
¤  Child abuse
¤  Acute psychosis NYD
¤  Altered LOC NYD
¤  Drug packer
65
Q

Which people should drink charcoal quickly?

A 
These People Should Drink Charcoal Quickly
Theophylline
Phenobarbital
Salicylates
Dapsone
Carbamazepine
Quinine
66
Q

what precautions do you use for a person WITH inhalational clostridium botulinum

A

standard

67
Q

Biological Weapon—?Clinical symptoms include constipation, dry mucous membranes, difficulty speaking and swallowing, and possibly, the absence of a gag reflex. Ptosis and extraocular muscle palsies may also be observed. Patients can develop respiratory distress.

A

inhalational c. botulinum

68
Q

t/f: Inhaled botulinum toxin cannot be spread by droplet or contact;

A

True

69
Q

cutaneous anthrax trt

A

cipro (teen)

70
Q

what is phosgene?

A

Pulmonary irritants cause pulmonary injury that may include cough, wheeze, dyspnea, hypoxia, and respiratory failure. Other pulmonary irritants include chlorine and ammonia, among others.

71
Q

Name two nerve agents and MOA

A

VX and sarin, are potent inhibitors of acetylcholinesterase and would also have effects on the CNS system and muscarinic receptors

72
Q

Name two Vesicants, what is a vesicant

A

sulfur mustard and Lewisite, would produce dermal damage as initial presenting symptoms.

73
Q

___ ____ is indicated for the treatment of internal contamination of cesium and thallium.

A

prussian blue

74
Q

Pneumonic plague is causd by _______ ______ and is shaped like a safety pin on Wright or Giemsa stain.

A

yersinia Pestis

75
Q

treat yersinia Pestis with

A

Gent or streptomycin

76
Q

intermittent apnea, increased nasal and oral secretions, respiratory distress, and vomiting. You note that they have small pupils, weakness, extremity tremors, and fasciculations

What toxidrome is caused by this nerve agent?

A

cholinergic

77
Q

intermittent apnea, increased nasal and oral secretions, respiratory distress, and vomiting. You note that they have small pupils, weakness, extremity tremors, and fasciculations

What’s the management?

A
78
Q

intermittent apnea, increased nasal and oral secretions, respiratory distress, and vomiting. You note that they have small pupils, weakness, extremity tremors, and fasciculations

Do you use physostigmine, diphendyramine, or pralixidone?

A

Pralixidone

79
Q

What are the antidotes for this toxidrome?

intermittent apnea, increased nasal and oral secretions, respiratory distress, and vomiting. You note that they have small pupils, weakness, extremity tremors, and fasciculations

A

atropine(antimuscarinic effects) and pralidoxime (a.k.a. 2-PAM),

80
Q

What does pralidoxime do?

A

which reactivates nerve transmission by attaching to the site where the nerve agent has attached and blocked cholinesterase. 2-PAM dislodges the nerve agent and removes it from cholinesterase, preserving the cholinesterase and allowing the enzyme to work normally again.

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