Toxicology Flashcards
List the toxidromes
Anticholinergic
s/s of anticholinergic
MAD AS A HATTER HOT AS A HARE DRY AS A BONE BLIND AS A BAT RED AS A BEET
Mental Status – altered
Eyes – midriasis
Skin – dry, flushed, hyperthermia, dry mucous membranes
GI/GU – decreased bowel sounds, urinary retension
Agent – antihistamines, atropine, scopolamine, tricyclic antidepressants
Treatment – physostigmine, sedation, cooling
Cholinergic
Skin – lacrimination, salivation
GI/GU – nausea, emesis, increased stooling and urination
Neuromuscular – muscle fasciculations, weakness
Lung – respiratory secretions
Heart – bradycardia
Agent – insecticides including carbamate, organophosphate, mushrooms
Treatment – atropine, pralidoxime, airway management and ventilatory support
Sympathomimetic
Mental Status – agitation
Heart – tachycardia, hypertension
Eyes – mydriasis
Skin – diaphoresis, hyperthermia
Agent – amphetamine, cocaine
Treatment – sedation, cooling, hydration
Hypoglycemic
Mental Status – altered
Heart – tachycardia, hypertension
Skin – diaphoresis
Mental Status – abnormal behavior, slurred speech, seizures
Agent – insulin, sulfonylureas
Treatment – glucose solutions intravenously or orally
Opioid
Mental Status – depressed
Lung – respiratory depression
Eyes – miosis
Skin – hypothermia
Agent – clonidine, heroin, morphine
Treatment – naloxone, respiratory support
Salicylates
Mental Status – altered Heart – tachycardia Lung – hyperpnea, respiratory alkalosis Skin – diaphoresis GI/GU – nausea, emesis
Agent – aspirin, wintergreen oil
Treatment – hydration, urine alkalinization, hemodialysis
Serotonin
Mental Status – altered especially agitation, hallucination
Neuromuscular – increased tone, hyperreflexia
Skin – hyperthermia
Neuromuscular – whole body tremors
Agent – SSRI, SSRI with other medications such as MAOI and TCAs, drugs of abuse including ectasy, LSD
Treatment – cooling, sedation, possibly cyproheptadine
Acetaminophen toxicity
Skin – diaphoresis GI/GU – anorexia, nausea, emesis Other Common Problems Mental Status – altered, agitated Heart – dysrhythmia Skin – jaundice GI/GU – hypoglycemia, hepatitis, pancreatitis, renal failure
Agent – acetaminophen
Treatment – N-acetyl choline
What are common medications poisonings?
Acetaminophen ASA Digoxin Theophylline Phenobarb Iron Lithium Methanol, Ethylene glycol
What is the antidote for Opiates?
Naloxone
What is the antidote for Benzodiazepines?
Flumazenil
What is the antidote for TCA, ASA?
Bicarbonate
What is the antidote for CCB?
Calcium
What is the antidote for Beta-blockers, CCB?
Glucagon
What is the antidote for Anticholinergics
Physostigmine
What is the antidote for Organophosphates, Carbamates?
Atropine
What is the antidote for Organophosphates
Protopam
What is the antidote for Methanol, ethylene glycol
Ethanol
What is the antidote for Acetaminophen
N-acetylcysteine
Describe acetominophen poisoning
7.5 and 15 grams in most adults
Clinical Presentation: (U of Alberta, Critical Care Medicine ppt)
Stage 1: Pre-injury period– 0-24h
Asymptomatic or minor N+V
Stage 2: Acute liver injury– 24-48h
RUQ pain, ↑AST/ALT, PTT, INR, bili +/- ↑Cr
Stage 3: Maximal liver injury – 48-96h
marked hepatic dysfn®fulminant hepatic failure, encephalopathy, coagulopathy, hypoglycemia, acidosis, renal failure
Stage 4: Recovery period - 4-14 days
Resolution of hepatic dysfunction and recovery
S/S of acetominophen poisoning
Lethargy -> encephalopathy -> death GI upset Diaphoresis Right upper quadrant pain Labs - Abnormal liver function tests - Prolonged prothrombin time - Increase bilirubin Hepatomegaly -> liver failure
Treatment of acetominophen overdose
Administer syrup of ipecac and follow emesis with activated charcoal
Prep for possible hemodialysis
This clears acetaminophen out but doesn’t stop the liver damage
Administer N-acetylcystein (NAC, Mucomyst) by IV
NAC replenishes essential liver enzymes - give q4h for 18 doses
Is most effective when started within 8 hours of ingestion
NAC is a glutathione precursor/substitute
Charcoal absorbs NAC, do not give together
S/S of ASA (salicyclates) by stage
Early - Tinnitus Significant - Nausea, vomiting - Hyperventilation/tachypnea ->respiratory alkalosis - Fever - Altered LOC - Hyperactivity -> lethargy - metabolic acidosis, ketosis Serious - Seizures - Rhabdomyolysis - Pulmonary edema - Cerebral edema - Acute renal failure - Respiratory failure - Coma - Death
S/S of ASA in general
Restlessness, tinnitus, deafness, blurring of vision
Hyperpnea, hyperpyrexia, sweating
Epigastric pain, vomiting, dehydration
Respiratory and metabolic acidosis
Disorientation, coma, cardiovascular collapse
CO poisoning toxicology
Normally, oxygen is carried through the bloodstream by hemoglobin (Hgb) in red blood cells. But since Hgb has a 200–250 times greater affinity (i.e., force to combine) for CO than for oxygen, introduction of CO into the bloodstream via the respiratory tract interferes with the oxygen-carrying capacity of blood. CO binds to Hgb, forming carboxyhemoglobin (COHb) and reducing the number of binding sites available for oxygen. As a result, there is a shift to the left in the oxyhemoglobin curve and tissue hypoxia occurs. In addition to its interference with tissue perfusion, CO has direct poisoning effects on the cellular level. Inhibition of the mitochondrial cytochrome oxidase system causes depression of cellular respiration. Direct binding of CO to cardiac myoglobin causes depression of cardiac function and muscle activity. CO also compromises the integrity of blood vessels, causing leakage of fluid into extravascular spaces.
Complications of CO poisoning
systemic acidosis, myocardial infarction (MI), rhabdomyolysis (i.e., acute renal failure resulting from renal tubule accumulation of byproducts from toxic destruction of skeletal muscle), pulmonary edema, and cerebral edema, which can cause retinal hemorrhage and papilledema.
S/S of CO poisoning
Early
- headache, dizziness, weakness, confusion, chest pain, nausea, and vomiting.
Severe
- hyperventilation, hypoxia, hypotension, and hyperreflexia develop
COHb levels
A normal COHb level in a healthy individual is < 3%; smokers may have COHb levels up to 10%
COHb level > 25% is dangerous, and COHb level > 50% can be fatal
S/S of cocaine overdose
Cocaine is a CNS stimulant that can:
- increase heart rate and blood pressure and
- cause hyperpyrexia,
- seizures, and
- ventricular dysrhythmias.
- intense euphoria,
- then anxiety, sadness, insomnia and sexual indifference;
- cocaine hallucinations with delusions;
Cocaine overdose management
Ensure airway and ventilation
control seizures
monitor cardiovascular effects;
have lidocaine and defibrillator available.
treat for hyperthermia
if cocaine was ingested, use charcoal to treat
S/S of opium overdose
Acute intoxication (overdose)
- Pinpoint pupils (may be dilated with severe hypoxia);
- Decreased blood pressure
- Marked respiratory depression
- Stuporà coma
- Fresh needle marks along course of any superficial verin; skin abscesses
Treatment of opiate overdose
1) support respiratory and cardioavascular functions
establish and IV line;
2) give narcotic antagonist (naloxone hydrochloride [Narcan]) as prescribed to reverse severe respiratory depression and coma
3) Hemodialysis may be indicated for severe drug intoxication.
4) maintain airway and provide respiratory support.
endotracheal intubation or tracheaostomy
5) hemodialysis
S/S of barbiturate overdose
Acute intoxication (may mimic alcohol intoxication):
- respiratory depression
- flushed face
- decreased pulse rate; decreased blood pressure
- increasing nystagmus
- depressed deep tendon reflexes
- decreasing mental alertness
- difficulty in speaking
- poor motor coordination
- coma, death
Treatment of barbiturate overdose
- maintain airway and provide respiratory support.
- large-gauge needle or IV catheter to support blood pressure;
- coma and dehydration result in hypotension and respond to infusion of IV fluids with elevation of blood pressure.
- Sodium bicarbonate may be prescribed to alkalinize urine; it promotes excretion of barbiturates.
- evacuate stomach contents or lavage as soon as possible to prevent absorption;
- repeated doses of activated charcoal may be administered.
- assist with hemodialysis for severely overdosed patient
maintain neurologic and vital sign flow sheet
S/S of Amphetamine-type Drug (Pep Pills, “Uppers,” “speed,” “crystal,” “meth”) overdose
Nausea, vomiting, anorexia, palpitations, tachycardia, increased blood pressure, tachypnea, anxiety, nervousness, diaphoresis, mydriasis Repetitive or stereotyped behaviour Irritability, insomnia, agitation Visual misperceptions, auditory hallucinations Fearful anxiety/depression, cold, distant hostility, paranoia Hyperactivity, rapid speech, euphoria Seizures, coma, hyperthermia,
Treatment of Amphetamine-type Drug
treat seizures with benzodiazepines
treat sympathetic stimulation with beta-blocker agents
S/S of alcohol withdrawl
nausea and vomiting, dyspepsia, headache, anorexia, sweating, tachycardia, hypertension, anxiety, agitation, tremors, vivid dreams, insomnia, tactile, visual and
auditory disturbances, hallucinations and delirium tremens. SEIZURES
Assessment of EtOH abuse
frequency of use,
usual quantity ingested,
duration of a drinking session,
date, time and amount of alcohol last used, and
any other drug use.
Assessment of withdrawl
> 20
10-20
7-10
1-6
Delirium Tremens (the DT’s)
is the most severe form of alcohol withdrawal and is a medical emergency.
a) Confusion and disorientation.
b) Extreme agitation or restlessness.
c) Gross tremor.
d) Autonomic instability (fluctuation in blood pressure & pulse, disturbances of electrolytes, hypothermia).
e) Paranoid ideation, typically delusional intensity.
f) Distractibility and accentuated response to external stimuli.
g) Hallucinations affecting any of the senses but typically visual.
h) Major psychotic disorders can sometimes mimic this state.
