Toxicology/Poisonings Flashcards

1
Q

Name some one-pill killers

One dose can be life threatening

A
Clonidine
Oil of wintergreen (methylsalicylate)
Camphor
Toxic alcohols (methanol, ethylene propyl)
TCAs
Benzocaine
CCBs
Sulfonylurea
Propanolol
Buprenorphine
Chlorpromazine
Chloroquine
Hydroxychloroquine
Lomotil
Methadone (and other opioids)
Quinidine
Quinine
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2
Q

What three treatments/antidotes should be considered in all comatose patients?

A

Oxygen
Glucose
Naloxone

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3
Q

Describe the following toxidrome: SYMPATHOMIMETIC

A

UPPERS

Agitation, Delirium, Psychosis, Seizure
Tachycardia
Hypertension
Fever/Hyperthermia
Mydriasis (increased pupil size - reactive)
Sweaty
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4
Q

Describe the following toxidrome: ANTICHOLINERGIC

A

Blind as a bat, hot as a hare, dry as a bone, red as a beet, mad as a hatter
The bowels and bladder lose their tone and the heart beats on alone

Delirium, Psychosis, Seizure, Coma/somnolence
Tachycardia
Hypertension
Fever/Hyperthermia
Mydriasis (increased pupil size - sluggish)
Decreased bowel sounds
Flushed/Dry skin

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5
Q

Describe the following toxidrome: CHOLINERGIC (ORGANOPHOPHATES)

A

Pouring with secretions

SLUDGE And the 3 killer B’s
DUMBELS

Salivation
Lacrimation
Urination
Diarrhea
GI Distress
Emesis
Bronchorrhea
Bradycardia
Bronchospasm
Diarrhea
Urination
Miosis
Bradycardia/Bronchorrea/Bronchospasm
Emesis
Lacrimation
Salivation
Fasiculations
Seizures
Can have tachycardiac (nicotinic) and bradycardia (muscarinic)
Normal or hypertension
Tachypnea
Miosis
Sweaty
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6
Q

Describe the following toxidrome: OPIATES (CLONIDINE)

A

DOWNERS

Somnolence/Coma
Tachycardia
Hypotension
Hypothermia
Bradypnea
Significant MIOSIS
Decreased bowel sounds
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7
Q

Describe the following toxidrome: SEDATIVE-HYPNOTICS (BARBITUATES)

A

ALSO DOWNERS

Somnolence/Coma
Hypotension
Hypothermia
Bradypnea
Bullae on skin (IV drug use)
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8
Q

Describe the following toxidrome: SALICYLATES

A
Coma/Somnolence, Seizures
Normal or tachycardia
Hyperthermia
Tachypnea
Sweaty skin
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9
Q

Name 3 differences between Sympathomimetics and Anticholinergics

A

Skin - Sweaty (SYM), Dry/flushed (ANTICHOL)
Pupils - Reactive (SYM), Sluggish (ANTICHOL)
Bowel sounds - No impact (SYM), Decreased (ANTICHOL)`

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10
Q

Bitter almond smell in your coffee - what toxin?

A

Cyanide

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11
Q

Name the toxins with characteristic smells

A
Cyanide - almonds
Arsenic, thallium, organophosphates, selenic acid - garlic
Chloral hydrate, paraldehyde - pears
Hydrogen sulfide - rotten eggs
Methyl salicylate - wintergreen
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12
Q

List the toxins that are poorly absorbed by activated charcoal

A

Heavy metals (Lithium, iron)
Alcohols
Hydrocarbons

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13
Q

List the possible indications for Whole Bowel Irrigation (WBI)

A
Body packers/stuffers
Ingestion of metals, lithium
Ingestion of sustained release preparations
Ingestion of pharmaceutical patches
Massive overdoses
Concretions of pills
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14
Q

List the possible indications for hemodialysis

A
Ethylene glycol
Lithium
Methanol
Salicylate
Theophylline
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15
Q

List some drugs that may lead to delayed expression of clinical toxicity

A
Sulfonylurea (oral hypoglycemics)
Acetaminophen
Iron
Sustained release drug formulations
MAOIs
Thyroid hormones
Warfarin
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16
Q

Toxic level for acetaminophen

A

150 mg/kg

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17
Q

Pathophysiology of acetaminophen poisoning

A

Acetaminophen saturates the hepatic metabolism pathways
Depletes glutathione
Causes increased production of NAPQi (N-acetyl-p-benzoquinone imine) - which binds to liver hepatocytes and causes necrosis

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18
Q

What are the 4 stages of acetaminophen poisoning?

A
STAGE 1         (30 min - 24 hours)
Asymptomatic, occasionally N/V, diaphoresis, pallor
STAGE 2        (24 - 48 hours)
N/V, RUQ abdo pain, elevates liver enzymes

STAGE 3 ( 72 - 96 hours)
Fulminant hepatic failure with jaundice, thrombocytopenia, increased INR, hypoglycemia, hepatic encephalopathy
Renal failure and cardiomyopathy may occur

STAGE 4
If patient survives - resolution of Sx

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19
Q

When do you draw an acetaminophen level?

A

at 4 - 24 hours post ingestion

Plot on the Rumack-Matthew nomogram to determine if antidote is required

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20
Q

What is the antidote for acetaminophen toxicity? How does it work

A
NAC 
N-acetyl-cysteine
Replenishes glutathione in the liver
Detoxifies the toxic metabolite - NAPQi
Alleviates existing hepatotoxicity through antioxidant and pro-circulatory properties

Effective when initiated within 8 hours of ingestion
Given IV over 21 hours (can be given PO - old regimen)
SE - anaphylactic reaction, reaction with pts with asthma

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21
Q

Describe the treatment for salicylate poisoning?

A

ABCDEF
Activated charcoal - in < 1-2 h post ingestion
IVF
Urine alkalinization - if peak level > 35 mg/dL (350 mg/L)
- reduces salicylate access to the brain
Hemodialysis - if patient meets these criteria: unremitting metabolic acidosis, pulmonary edema, severe renal impairment, coma, seizures, liver impairment, salicylate level > 70 mg/dL (700 mg/L)

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22
Q

What hazard is associated with intubation of salicylate poisoned patients?

A

Tend to have profound respiratory alkalosis
Abrupt reversal with a sedative and paralytic - causes significant acidemia which may increase salicylate entry to the brain and cause seizures

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23
Q

How does iron produce toxicity?

A

Iron acts on the GI mucosa
Inhibits oxidative phosphorylation in the mitochondria
Body has no mode of excretion of excess iron

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24
Q

What are the toxic levels of iron?

A
Ingestion levels:
Mild: 20 - 60 mg/kg
Moderate: 60 - 100
Serious: 100-200
Lethal : > 200

Serum levels roughly correlate with toxicity:
< 350 mcg/dL – minimal
350-500 mcg/dL – mild
>500 mcg/dL – serious

Check serum iron levels 4-6 hours post ingestion
AXR - can sometimes show iron pills that have not been absorbed yet

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25
Q

What are the stages of Iron toxicity?

A

STAGE 1 (up to 6 hours)
GI Symptoms, N/V, GI bleed
If severe - shock due to volume loss, coma

STAGE 2 (6 - 24 hours)
GI Symptoms resolve, patient looks relatively well
Transient phase

STAGE 3        (>24 hours)
Metabolic acidosis, hepatocellular injury, elevated transaminases, jaundice, intractable shock, seizures, coma
STAGE 4          (4-6 weeks)
Resolution of symptoms, patients who survive can get gastric scarring and cause pyloric stenosis
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26
Q

What is the antidote for iron poisoning?

A

Deferoxamine

An iron chelator

Dose: 5-15 mg/kg/hour (up to 6g/day) IV
Stop it for 6 h q24h - to prevent ARDS or pulmonary fibrosis

Causes vin-rose urine

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27
Q

What reasons would you stop deferoxamine?

A

Clinical improvement:
Urine runs clear
Metabolic acidosis resolves
Iron level returns to normal

Adverse effects:
Anaphylactic reaction
ARDS
Pulmonary fibrosis
Cramps
Neuropathy
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28
Q

What gastrointestinal decontamination is helpful and what is not helpful in iron toxicity?

A

Helpful - WBI - if undissolved tabs on AXR, or massive overdose

Not- helpful - activated charcoal

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29
Q

List the major toxicities of TCAs

A
Na channel blockade - in the cardiac conduction system - dysrhythmias
Seizures
alpha blockade - hypotension
Inhibition of NE reuptake
Anticholinergic toxicity
30
Q

What ECG findings correlate with TCA toxicity?

A

Wide QRS > 100 ms
Prolonged QT
R wave height greater than 3 mm in lead aVR

31
Q

How does bicarb improve the QRS interval in TCA toxicity?

A

Na Bicarb competitively inhibits the Na blockade by increasing available serum sodium
Also the serum alkalinization promotes improved conduction that narrows the QRS and causes cessation of the ventricular tachycardia

32
Q

What drugs cause bradyarrhythmias?

What are helpful antidotes?

A

Beta blockers
CCB
Digoxin-containing compounds

Not amenable to atropine, epinephrine and pacing

Beta blockers: Glucagon, lipid emulsions
CCB: Calcium, insulin/glucose, lipid emulsions
Digoxin: Digi-Fab

33
Q

What is flumazenil an antidote for and what are the concerns for using it?

A

Benzos
Benzo-receptor antagonist

May precipitate benzo withdrawal
May precipitate seizures and their complications
Short duration of action compared with duration of benzo toxicity

34
Q

How do you treat seizures from an overdose/toxic exposure?

A

Benzos
Barbituates
Pyridoxine - isoniazid overdose

Don’t use:
Phenytoin - Na channel issue - can complicate TCA toxicity

35
Q

Signs and Sx of isolated benzo overdose

A

Sedation
Ataxia
Respiratory depression

Apnea
Deep coma
Cardiovascular instability
THINK COINGESTANTS - ethanol, barbituates, other sedative-hypnotics

36
Q

Toxidrome for opioid toxicity

A

FAME

Flaccid coma
Apnea
Miosis
Extraocular paralysis

Causes global depression of central and autonomic nervous systems

37
Q

Antidote for opioid toxicity?

A

Naloxone

May need higher doses for - methadone, LAAM, dextromethorhan, pentazocine, fentanyl
OR
Smaller doses for - people habituated to opioid use

38
Q

What drug mimics opioid toxicity but does not respond to naloxone?

A

Clonidine

Alpha-adrenergic agonist
Acts centrally to reduce sympathetic outflow

39
Q

Signs and Sx of clonidine poisoning

A
Miosis
Coma
Apnea
Bradycardia
Hypotension
Transient arousal with stimulation

As little as 0.1 mg (1 tablet)

40
Q

Which drugs can cause hallucinations or psychosis?

A

Anticholinergics (antihistamines, Jimson weed)
Dissociatives (phenycyclidine, ketamine, dextromethrophan)
Hallucinogens (LSD, psilocybin, mescaline)
Sympathomimetics (amphetamines, cocaine, MDMA-ecstasy, bath salts, synthetic cannabinoids - spice, K2)
Withdrawal from ethanol or sedative-hypnotics

41
Q

Why don’t we use haloperidol for sedation?

A

May lower the seizure threshold
May add to the cardiotoxicity of some drugs
May limit the patient’s ability to dissipate heat

42
Q

Signs and Sx of cocaine toxicity

A
Initial rush of euphoria and increased energy
Agitation
Tachycardia
Hypertension
Hyperthermia
Mydriasis
Tremor
Seizures
Intracranial hemorrhage
Myocardial ischemia
Rhabdomyolysis
Pneumothorax
Psychosis
Death
43
Q

What treatments are effective in cocaine toxicity?

A

Benzos for agitation, seizures, tachycardia
Environmental cooling for hyperthermia
Mechanical ventilation, paralysis, and bicarb for rhabdomyolysis to reduce chance of renal failure
Nitroprusside infusion for hypertension

Reserve sympatholytics

Do not use Beta blockers

44
Q

Name 7 hyperthermic syndromes in toxicology

A
Anticholinergics
Sympathomimetics
Neuroleptic Malignant Syndrome
Malignant hyperthermia
Serotonin syndrome
Salicylate poisoning (due to the uncoupling of oxidative phosphorylation)
Acute withdrawal syndrome
45
Q

Signs and Sx of Serotonin syndrome

A

Autonomic hyperactivity
Increased neuromuscular tone
Hyperreflexia
CNS depression

46
Q

Methods of abusing inhalants

A

Sniffing
Huffing
Bagging

Inhaled hydrocarbons - cause ventricular dysrhythmias - especially if agitated - due to increased catecholamine cardiac activity
In resusc of these patients - use Beta blockers rather than epi

47
Q

Signs and Sx of synthetic cannabinoids

A
Aggressive behaviour
Paranoia
Dystonia
Prolonged psychosis
Seizures
AKI
MI
48
Q

Signs and Sx of bath salt intoxication

A

Synthetic cathinones
Like amphetamines

Prolonged agitation
Aggressive and violent behaviour
Hallucinations
Paranoia
Seizures
49
Q

DDX of increased anion gap metabolic acidosis

A

MUDPILES

Methanol, metformin
Uremia
DKA - Diabetic, alcohol and starvation ketoacidosis
Paraldehyde
Isoniazid, Iron, Inborn errors of metabolism
Lactic acidosis
Ethylene glycol
Salicylate

Lactic acid can be caused by sepsis, shock, seizures, anoxia, ischemia, trauma, toxins (CO, cyanide, sodium azide, hydrogen sulfide, ibuprofen, adrenergic agents, isoniazid, etc.)

50
Q

Osmolar gap calculation, normal range, and DDx of large osmolar gas

A

Osmolar gap = Measured Osm - Calculated Osm

Calculated Osm = 2Na + Glu + BUN

Normal -7 to 10 mOSM

DDx:
Acetone
Ethanol 
Gylcols
Isopropanol
Magnesium
Mannitol
Methanol
Renal failure
Severe ketoacidemia
Severe lactic acidosis
51
Q

Why do kids have such severe hypoglycemia from ethanol intoxication?

A

Ethanol breakdown inhibits gluconeogenesis
Kids have poor glycogen stores
No glucose produce, all glucose used = hypoglycemia

Ethanol is metabolized by the enzymes alcohol dehydrogenase and acetaldehyde dehydrogenase – produces NADH (from NAD)

Higher ratio of NADH>NAD - inhibits gluconeogenesis

52
Q

Rate of ethanol metabolism

A

15 mg/dL/hour

53
Q

How do you treat toxic alcohol poisoning

A

Ethanol
Fomepizole

Aim is to inhibit alcohol dehydrogenase - so it doesn’t breakdown the toxic alcohol (methanol, or ethylene glycol) - which produces formic acid (toxic to retina) and oxalic and glycolic acids (toxic to kidneys)

Supplements:
Folic acid (promotes breakdown of formic acid)
Pyridoxine and thiamine (speeds breakdown of glycolic acid - into nontoxic metabolites)
54
Q

What characteristics of a caustic agent are most predictive of injury

A
pH
Concentration
Volume ingested
Viscosity of product
Manner of exposure
Duration of exposure
55
Q

Complications of caustic agent ingestion

A
ACUTE:
Upper airway obstruction
Aspiration pneumonitis
GI bleeding or perforation
Systemic acidosis or DIC
Sepsis
CHRONIC:
Esophageal stricture
Impaired GI function
Pyloric obstruction
Esophageal carcinoma - 1000 fold increased risk
56
Q

Indications to scope after caustic ingestion

A

Ingestion of a concentrated strong acid or base
Suicidal ingestion
Large volume
Patients with vomiting or >2 signs of injury

57
Q

Indications for surgical exploration following caustic ingestion

A

Evidence of perforation
Abdominal tenderness after acid ingestion
Inability to evaluate injuries endoscopically
Significant CNS depression
Progressive metabolic acidosis
Hypotension with tachycardia

58
Q

Hydrocarbon characteristics that make them prone to aspiration

A

Low viscosity
Low surface tension
High volatility

59
Q

Describe the time course for developing aspiration injury after hydrocarbon ingestion

A

Pneumonitis - 6 hours

98% by 24 hours

60
Q

Signs and symptoms of severe systemic toxicity from hydrocarbon ingestin

A
CNS depression
Seizures
Hepatotoxicity
Nephrotoxicity
Bone marrow toxicity
61
Q

Hydrocarbons noted for systemic toxicity

A

CHAMP

Camphor
Halogenated hydrocarbons 
       (carbon tetrachloride, trichloroethane)
Aromatic hydrocarbons (benzene, toluene)
Metal-containing hydrocarbons
Pesticide containing hydrocarbons
62
Q

How do you manage a child who ingests anticoagulant rodenticide

A

Activated charcoal
Do INR 2-3 days later

If severe coagulatopathy - large amount or chronic ingestion
Give Vit K
FFP

If superwarfarin - needs monitoring for 5 days

63
Q

Signs and Sx of CO poisoning

A

Malaise
Nausea
Lightheadedness
Headache

More severe can lead to:
Confusion
Coma
Syncope
Seizure
Death

Survivors:
Cognitive defects
Personality changes
Movement disorders

64
Q

Who is most affected by CO poisoning?

A

Infants/small children

Higher O2 consumption
Higher basal metabolic rate

65
Q

How long does it take the body to eliminate Carboxyhemoglobin?

A

Depends on inspired oxygen concentration

RA 4-6 hours
100% O2 40-90 minutes
Hyperbaric O2 (3 atm) 15-30 mins

66
Q

Criteria for hyperbaric oxygen

A

Syncope
Confusion
CNS depression
Very high carboxyhemoglobin levels

67
Q

Cyanosis that is unresponsive to supplemental oxygen with a normal partial pressure of oxygen on arterial blood gas

A

Methemoglobinemia

When the iron is Ferric (3+) rather than Ferrous (2+) - can’t transport oxygen

68
Q

DDx for methemoglobinemia

A

CONGENITAL
Hemoglobin M
NADH
Cytochrome b5 reductase deficiency

ACQUIRED
Transient, illness-associated methemoglobinemia of infancy
Toxicant induced

Transient illness associated in infants - due to diarrheahl dehydration, metabolic acidosis, UTI and other illnesses - anything causing oxidative stress

Toxins - benzocaine, dapsone, environmental nitrates (well water), nitrites (amyl nitrite), and phenazopyridine

69
Q

Treatment for methemoglobinemia

A

Supplemental oxygen
Eliminate or treat oxidative stress
Methylene blue (1-2 mg/kg of 1% solution) - except in G6PD

70
Q

What feature distinguishes toxic from GI irritant mushrooms

A

Time course of vomiting

Delayed vomiting - >6 hours post ingestion - is BAD

71
Q

Name toxic mushroom classes and their target toxicity

A

SEVERE (Vomiting > 6h post ingestion)
Gyromitra - inhibits pyridoxine phosphokinase
Orellanine - nephrotoxic
Amanita + Galerina + Lepiota - hepatotoxic

SEVERE (Vomiting <6h)
Amanita smithiana - nephrotoxic

MILD (Vomiting or Sx begin < 6h)
Psilocybe - magic mushroom - serotonin
Ibotenic acid (Amanita muscaria) - GABA, glutamatergic
Coprine (inky cap) - Disulfiram-like
Emetogenic mushrooms - gastric irritants
Muscarinic - cholinergic
Mytotoxic - rhabdomyolysis
72
Q

Name some toxic plants by symptoms class, plants, potential treatment

A

SYMPTOM CLASS : Plants - (Tx)
GI irritants: Pokeweed, horse chestnut, english ivy
(Supportive care)

Toxalbumin: castor bean, rosary pea, autumn crocus (colchicine containing)
(Supportive care for multisystem organ failure)

Digitalis-like toxin: Foxglove, oleander, lily of the valley
(Digoxin Fab fragments - Digifab)

Cardiac effects: Mistletoe, monkshood, false hellebore, mountain laurel
(Supportive care, standard treatment of dysrhythmias)

Nicotinic effects: Wild tobacco, tobacco, poison hemlock
(Atropine, supportive care for weakness, paralysis)

Anticholinergic effects: Jimson weed, Angel’s trumpet, Matrimony vine, henbane, belladonna
(Physostigmine for seizures, malignant hyperthermia
Benzos for delirium)

Seizures: Water hemlock (Anticonvulsants)

Hallucinations: Morning glory, nutmeg, peyote (Sedation)

Cyanogenic: Chokecherry, pits (cherry, plum, peach), seeds (apple, pear), cassava, elderberry (leaves/shoots), black locust
(Cyanide antidote - rarely needed)