Medicinal Poisons

Prepared by: Kristine Mae F. Gante, RPh

AMPHETAMINE
Activates the sympathetic
nervous system
stimulation, peripheral
release of
cathecolamines, or
monoamine oxidase
AMPHETAMINE
Clinical Findings
Acute Poisoning:
Inhalation or injection of
decomposed epinephrine
may cause a psychosis-like
state with hallucinated
and morbid fears.
AMPHETAMINE
Clinical Findings
Chronic Poisoning:
Emotionally unstable
individuals may lead to
personality changes with
psychic craving
AMPHETAMINE
Clinical Findings
Chronic Poisoning:
Tension or anxiety
progressing to psychosis
AMPHETAMINE
Clinical Findings
Chronic Poisoning:
Long-term use of
Dextroamphetamine for
control of hyperactivity in
children causes growth
retardation
AMPHETAMINE
Prevention
Warn the adults/parents
of the dangers of
incautious administration
of potent nose drops to
infants.
AMPHETAMINE
Treatment:Acute Poisoning
Emergency measures:
Cyanosis artificial
respiration
AMPHETAMINE
Treatment:Acute Poisoning
Emergency measures:
Remove drug by ipecac
emesis followed by
activated charcoal
AMPHETAMINE
Treatment:Acute Poisoning
Antidote:
Chlorpromazine (for pure
amphetamine poisoning)
0.5-1 mg/kg every 30
minutes as needed
AMPHETAMINE
Treatment:Acute Poisoning
Antidote:
Droperidol (useful for
amphetamine and
methampethamine)
2.5 mg/min to a total of
10-15 mg
AMPHETAMINE
Treatment:Acute Poisoning
General Measures:
Control convulsion
Acid diuresis
(amphetamine and
methampethamine)
DISULFIRAM
BN: Antabuse
Antioxidant

Used in the treatment of

alcoholism
DISULFIRAM
It
is taken orally.
Well-absorbed

Highly lipid-soluble
DISULFIRAM
Mechanism of Toxicity
A. Irreversible inhibition of
aldehyde dehydrogenase
DISULFIRAM
Mechanism of Toxicity
DISULFIRAM
Mechanism of Toxicity
B. Depletion of
Norepinephrine in terminal
presynaptic nerve ending
causing orthostatic
hypotension
DISULFIRAM
Mechanism of Toxicity
C. Long-term use may cause
peripheral neuropathy due
to its metabolite carbon
disulfide
DISULFIRAM
Toxic Dose
A. Disulfiram Overdose
Ingestion of 3 grams or
more may cause toxicity
DISULFIRAM
Toxic Dose
A. Disulfiram-Ethanol
Interaction
Ingestion of as little as 7mL of
ethanol can cause severe
reactions in patients taking
as little as 200 mg/day of
disulfiram.
DISULFIRAM
Clinical Presentation
The most common side
effects (in the absence of
alcohol)
drowsiness, headache, and
a metallic or garlic taste in
the mouth.
DISULFIRAM
Clinical Presentation
Tryptophol is a chemical
compound that induces
sleep in humans.
DISULFIRAM
Clinical Presentation
The accumulated
acetaldehyde exerts its
toxic effects by inhibiting
the mitochondrial
reactions and functions.
DISULFIRAM
Clinical Presentation
The accumulated
acetaldehyde causes
further liver damage--
hepatitis and cirrhosis.
ANTINEOPLASTIC
AGENTS
Toxic effects are
extensions of the
pharmacologic properties
of the drugs.
ANTINEOPLASTIC
AGENTS
Alkylating Agents
These drugs provide highly
charged carbon atoms that
attack nucleophilic sites on
the DNA, resulting in
alkylation and cross
stranding; thus inhibiting
replication and transcription.
ANTINEOPLASTIC
AGENTS
Alkylating Agents
Binding to RNA or
protein moieties appears
to contribute little to toxic
effects
ANTINEOPLASTIC
AGENTS
Antibiotics
These drugs intercalate
within base pairs in DNA-
directed RNA synthesis.
Toxicity: generation of
cytotoxic free radicals
ANTINEOPLASTIC
AGENTS
Antimetabolites
They interfere with DNA
synthesis at various stages.
ANTINEOPLASTIC
AGENTS
Hormones
Steroid hormones regulate
the synthesis of steroid-
specific proteins.
The exact mechanism of
antineoplastic action is
unknown.
ANTINEOPLASTIC
AGENTS
Mitotic Inhibitors
Inhibits mitosis, thereby
arresting cell division
ANTINEOPLASTIC
AGENTS
Clinical Presentation
Leukopenia
Most common
manifestation of toxicity
from antineoplastics is
bone marrow depression.
ANTINEOPLASTIC
AGENTS
Clinical Presentation
GI Manifestations
Nausea, vomiting,
diarrhea, severe ulcerative
gastritis, extensive fluid loss
BETA-ADRENERGIC
BLOCKERS
Mechanism of Toxicity:
Excessive beta-adrenergic
blockade
BETA-ADRENERGIC
BLOCKERS
Mechanism of Toxicity:
Propranolol and other
agents with membrane
depressant
Depresses myocardial
contractility and
conduction
BETA-ADRENERGIC
BLOCKERS
Mechanism of Toxicity:
Propranolol
It is lipid soluble; thereby
enhances brain
penetration can cause
seizures and coma.
BETA-ADRENERGIC
BLOCKERS
Mechanism of Toxicity:
Pindolol
Partial beta-agonist
activity
It may cause
hypertension.
BETA-ADRENERGIC
BLOCKERS
Mechanism of Toxicity:
Sotalol
Has type III antiarrythmic
activity
Prolongs QT interval causing
torsades de pointes and
ventricular fibrilation
BETA-ADRENERGIC
BLOCKERS
Clinical Presentation:
Cardiac Disturbances
CNS Toxicity
Bronchospasms
Hypoglycemia
Hypokalemia
BETA-ADRENERGIC
BLOCKERS
Treatment:
Emergency
and Supportive Measures
ABCs of life suport
Treat coma, seizures,
hypotension,
hyperkalemia, and
hypoglycemia
BETA-ADRENERGIC
BLOCKERS
Treatment: Emergency and
Supportive Measures
Bradycardia:
Atropine (0.01-0.03 mg/kg IV)
Isoproterenol
Cardiac pacing
BETA-ADRENERGIC
BLOCKERS
Treatment: Emergency and
Supportive Measures
Bronchospasm:
Nebulized bronchodilators
Aminophylline for beta-blocker
induced wheezing
BETA-ADRENERGIC
BLOCKERS
Specific Drugs/ Antidotes

Glucagon
For bradycardia and
hypotension
5-10 mg IV bolus, repeated as
needed and followed by an
infusion of 1-5mg/h
BETA-ADRENERGIC
BLOCKERS
Specific Drugs/ Antidotes

Epinephrine
IV infusion starting at 1-4
mcg/min
BETA-ADRENERGIC
BLOCKERS
Specific Drugs/ Antidotes

Torsades de pointes
Magnesium
Isoproterenol
Correction of hypokalemia
CALCIUM ANTAGONISTS
Mechanism of Toxicity
Calcium antagonists slow
the influx of calcium
through cellular calcium
channels.
CALCIUM ANTAGONISTS
Site
of Action: vascular
smooth muscles, cardiac
muscles
CALCIUM ANTAGONISTS
Clinical Presentation
Hypotension
Caused by peripheral
vasodilation, reduced cardiac
contractility, slowed HR
CALCIUM ANTAGONISTS
Clinical Presentation
Bradycardia
May result from sinus
bradycardia, 2nd or 3rd
degree AV block, sinus arrest
with junctional rhythm
CALCIUM ANTAGONISTS
Clinical Presentation
Noncardiac Manifestations
Nausea and vomiting
Abnormal mental status
Metabolic acidosis
Hyperglycemia
CALCIUM ANTAGONISTS
Treatment
Calcium
Reverses the depression of
cardiac contractility but have
no effect on sinus node
depression or peripheral
vasodilation
CALCIUM ANTAGONISTS
Treatment
Calcium
Calcium chloride
Calcium gluconate
CALCIUM ANTAGONISTS
Treatment
Hypotension and Bradycardia
Glucagon
Epinephrine
Amrinone
Medicinal Poisons
Beta-AdrenergicBlockers
Calcium Antagonists

Captopril and Related

Drugs
ACE-INHIBITORS
Mechanism of Toxicity
Inhibits the
peptidyldipeptide
carboxyhydrolase
(angiotensin-converting
enzyme)
ACE-INHIBITORS
Clinical Presentation
Mild hypotension
Bradycardia
Persistent coughing
Angioedema
CLONIDINE
Centrally-acting adrenergic drugs
Clonidine
Guanabenz
Hypertension
Guanfacine
Methyldopa
Nasal
Oxymetazoline
Decongestants
Tetrahydrozoline
Tizanidine Muscle spasms
CLONIDINE
Mechanisms of Action
Allthese agents decreases
sympathetic outflow by
stimulating alpha-2 receptors
in the brain.
CLONIDINE
Mechanisms of Toxicity
Clonidine,Oxymetazoline,
Tetrahydozoline
Stimulates peripheral alpha-1
receptors, resulting in
vasoconstriction, and
transient hypertension
CLONIDINE
Mechanisms of Toxicity
Guanabenz

Ganglionic blocker
CLONIDINE
Mechanisms of Toxicity
Methyldopa

May further decrease

sympathetic outflow by
metabolism to false
neurotransmitter, alpha-
methylnorepinephrine
CLONIDINE
Mechanisms of Toxicity
Methyldopa

Decreases plasma renin

CLONIDINE
Clinical Presentation
Generalized sympathetic
depression
CLONIDINE
Treatment
Naloxone
Reverses the toxicity of
clonidine
MOA is unknown
CLONIDINE
Treatment
Tolazoline
Central alpha-2 receptor
antagonist
DEXTROMETHORPHAN
Mechanism of Action
Antitussive
It is the d-isomer of 3-
methoxy-N-
methylmorphinan, a
synthetic analogue of
codeine.
DEXTROMETHORPHAN
Mechanism of Action
L-isomer is Levorphanol
(opioid analgesic)
DEXTROMETHORPHAN
Mechanism of Action
Dextromethorphan has an
equal antitussive efficacy
with codeine
It has no analgesic or
addictive properties
DEXTROMETHORPHAN
Mechanism of Action
Produces mild opioid
effects
DEXTROMETHORPHAN
Mechanism of Toxicity
Dextrometorphan and its
o-demethylated
metabolite antagonizes
NMDA glutamate
receptors (Anticonvulsant
properties)
DEXTROMETHORPHAN
Mechanism of Toxicity
It inhibits serotonin
May lead to serotonin
syndrome in patients
taking MAOIs
DEXTROMETHORPHAN
Mechanism of Toxicity
Dextrometorphan HBr
may cause Bromide
poisoning
DEXTROMETHORPHAN
Clinical Presentation
Mild Intoxication
Clumsiness, ataxia,
nystagmus, restlessness,
visual and auditory
hallucinations
DEXTROMETHORPHAN
Clinical Presentation
Severe Poisoning
Stupor, coma, respiratory
depression, seizures,
dilation of pupils
DEXTROMETHORPHAN
Clinical Presentation
Serotonin Syndrome
Severe hyperthermia
Muscle rigidity
Hypertension
DEXTROMETHORPHAN
Treatment
Naloxone
0.06 0.4 mg
ISONIAZID
A hydrazide derivative of
isonicotinic acid
Bactericidal drug of
choice for TB
ISONIAZID
Mechanism of Toxicity
Acute Overdose
Itcompetes with the
pyridoxal 5-phosphate in
the brain, the active form of
Vitamin B6 for the enzyme
glutamic acid decarboxylase
ISONIAZID
Mechanism of Toxicity
Acute Overdose
This
results in lower levels
of GABA
ISONIAZID
Mechanism of Toxicity
Acute Overdose
Isoniazid also inhibits the
hepatic conversion of
lactate to pyruvate,
leading to lactic acidosis
ISONIAZID
Mechanism of Toxicity
Chronic Toxicity
Peripheral neuritis is due to
the competition with
pyridoxine
ISONIAZID
Treatment
Pyridoxine
5 g IV if the amount of INH is
unknown
If the amount of INH is
known, give an equivalent
amount in grams of
Pyridoxine
LOMOTIL & OTHER
ANTIDIARRHEALS
Itis a combination
product containing
Diphenoxylate and
atropine that is
commonly prescribed for
the symptomatic
treatment of diarrhea.
LOMOTIL & OTHER
ANTIDIARRHEALS
Loperamide
Is a nonprescription drug
with similar properties.
LOMOTIL & OTHER
ANTIDIARRHEALS
Mechanism of Toxicity
Diphenoxylate
Opioidanalog of
meperidine
LOMOTIL & OTHER
ANTIDIARRHEALS
Mechanism of Toxicity
Diphenoxylate
Metabolite: Difenoxin
Has five-fold antidiarrheal
activity
LOMOTIL & OTHER
ANTIDIARRHEALS
Clinical Presentation
Opioid Intoxication
Pupilconstriction
Coma

Respiratory arrest
LOMOTIL & OTHER
ANTIDIARRHEALS
Treatment
Naloxone
1-2 mg IV
LOMOTIL & OTHER
ANTIDIARRHEALS
Treatment
Physostigmine
Itmay reverse signs of
anticholinergic poisoning
LSD & OTHER
HALLUCINOGENS
Mechanisms of Toxicity
The biochemical
mechanism of
hallucinations is not
known
LSD & OTHER
HALLUCINOGENS
Mechanisms of Toxicity
LSD stimulates 5-HT2
receptors
LSD & OTHER
HALLUCINOGENS
Clinical Presentation
Mild to Moderate
Intoxication
Mild psychosis
LSD & OTHER
HALLUCINOGENS
Clinical Presentation
Life-threatening Toxicity
Intense sympathomimetic
stimulation
LSD & OTHER
HALLUCINOGENS
Clinical Presentation
Life-threatening Toxicity
Seizures

Hyperthermia

Hypertension

Cardiac arrhythmias
LSD & OTHER
HALLUCINOGENS
Treatment
There is no specific
antidote
LSD & OTHER
HALLUCINOGENS
Treatment
Sedating doses of
DIAZEPAM may alleviate
anxiety
2-10 mg
LSD & OTHER
HALLUCINOGENS
Treatment
Hypnotic doses of
DIAZEPAM may induce
sleep for the duration of
the trip (4-10h)
10-20 mg
LSD & OTHER
HALLUCINOGENS
Examples of Hallucinogen
Bufotenine
From the skin secretions of
the toad Bufo vulgaris
LSD & OTHER
HALLUCINOGENS
Examples of Hallucinogen
DMT
Dimethyltryptamine

Businessmans trip
LSD & OTHER
HALLUCINOGENS
Examples of Hallucinogen
Mescaline
Derived from peyote cactus
LSD & OTHER
HALLUCINOGENS
Examples of Hallucinogen
Psilocybin
From Psilocybe mushroom
Specific overdoses
Opiates
Antidote naloxone
MOA: Pure opioid antagonist
competes and displaces narcotics
at opioid receptor sites
Lower doses in opiate dependence
S/E BP changes; arrhythmias;
seizures; withdrawal
Benzodiazepines

Antidote flumazenil
MOA: Benzodiazepine antagonist
IV administration 0.2 mg over 15
sec to max 3mg
S/E N&V; arrhythmias;
convulsions
Salicylate overdose

Aspirin (acetylsalicylic acid)

Methyl salicylate (Oil of Wintergreen)
5 ml = 7g salicylic acid
Herbal remedies
Fatal intoxication can occur after the
ingestion of 10 to 30 g by adults and
as little as 3 g by children
Clinical features

Early symptoms of aspirin toxicity include

tinnitus, fever, vertigo, nausea,
hyperventilation, vomiting, diarrhoea

More severe intoxication can cause altered

mental status, coma, non-cardiac pulmonary
oedema and death
Salicylate overdose - treatment

directed toward increasing systemic pH by the

administration of sodium bicarbonate

IV fluids +/- vasopressors

Avoid intubation if at all possible ( acidosis)

Supplemental glucose (100 mL of 50 percent

dextrose in adults) to patients with altered mental
status regardless of serum glucose concentration to
overcome neuroglycopaenia
Hemodialysis
 Drug Abuse

Self administration of drug or drugs

in manner not in accord with accepted
medical or social patterns
Drug Abuse

Psychological Dependency
(Habituation)
Drug necessary to maintain users
sense of well-being

Physical Dependency
Physical symptoms if intake reduced
Drug Abuse

Compulsive Drug Use

Preoccupation with obtaining drug
Rituals of preparing, using drug as
important as drug effects

Tolerance
Increasing doses needed to obtain
drug effect
Drug Abuse

Addiction
Includes
Psychological dependence
Physical dependence

Compulsive use

Tolerance
Narcotics

Opium
Opium derivatives
Synthetic opium substitutes
Narcotics

Examples
Oxycodone (Percodan)
Opium
Meperidine (Demerol)
Morphine
Propoxyphene
Heroin (Darvon)
Codeine Talwin

Dilaudid Fentanyl
Krocodil

Flesh eating drug

Narcotics
Effects
Analgesia
CNS depression
Euphoria

Drowsiness

Apathy

Antidiarrheal action
Antitussitive action
Narcotics
Withdrawal
Insomnia Watery eyes
Restlessness Yawning

Irritability Rhinorrhea

Anorexia Sneezing

Tremors Diarrhea

Back, extremity pain Diaphoresis

Resembles Severe Influenza

Sedative-Hypnotic Drugs
Categories
Barbiturates
Benzodiazepine
Barbiturate-like non-barbiturates
Chloral hydrate
Barbiturates
Introduced in 1903
Replaced older sedative-hypnotics
Quickly became major health problem
In 1950s-60s barbiturates were implicated
in overdoses; were responsible for majority
of drug-related suicides
Barbiturates
Short-acting
Amytal
Pentathiol

Intermediate-acting
Nembutal
Seconal
Tuinal

Long-acting
Phenobarbital
Barbiturate-like, non-barbiturates
Examples
Doriden (glutethimide)
Quaalude (methaqualone)
Placidyl (ethchlorvynol)
Noludar

Overdose produces sudden, prolonged apnea

Highly addictive
Withdrawal resembles barbiturate withdrawal
Only Placidyl, Doriden remain available in U.S.
Benzodiazepines
Developed due to overdoses, deaths related
to barbiturates, barbiturate-like non-
barbiturates
Relatively few deaths
In 1993, prescription rate for barbiturates
dropped to one-sixth that of benzos
Benzodiazepines
Examples
Valium (diazepam)
Ativan (lorazepam)
Versed (midazolam)
Librium (chlorodiazepoxide)
Tranxene (chlorazepate dipotassium)
Dalmane (flurazepam)
Halcion (triaxolam)
Restoril (temazepam)
Benzodiazepines
Produce withdrawal syndrome similar to
barbiturate withdrawal
Benzodiazepine-like non-benzos
BuSpar (buspirone)
Used for generalized anxiety disorder
Less sedating than diazepam
Less potentiation by other CNS depressants

Ambien, Stilnox (zolpidem)

Used for short-term insomnia treatment
Toxic effects similar to benzos
Neuroleptics
Antipsychotics, major tranquilizers
Used in treatment of schizophrenia, other
psychoses
Examples
Haldol
Mellaril
Thorazine
Stellazine
Compazine
Neuroleptics
Extrapyramidal muscle contractions
(dystonias)
Bizarre, acute, involuntary movements, spasms
of skeletal muscles
Reversible with Benadryl
Stimulants
Examples
Cocaine
Amphetamines
Benzedrine (bennies)
Dexedrine (dexies, copilots)

Methamphetamine (ice, black beauties)

Ephedrine
Caffeine
Ritalin
Stimulants
Produce
euphoria
hyperactivity
alertness
senseof enhanced energy
anorexia
Hallucinogens

Examples
Indole hallucinogens Amphetamine-like

LSD (acid)
hallucinogens
Peyote
Morning-glory
seeds Mescaline

Psilocybin DOM

DMT MDA

MDMA (ecstasy)
Hallucinogens
Some patients may experience bad trips
Depends on surroundings, emotional state
Signs and symptoms
Paranoia, fearfulness, combativeness
Anxiety, excitement
Nausea, vomiting
Tachycardia, tachypnea
Tearfulness
Bizarre Reasoning
Phencyclidine (PCP)
Street names
Angel dust
Peace Pill
Hog
Krystal
Animal tranquilizer
Used as veterinary anesthetic
Date rape drugs
Flunitrazepam (Rhohypnol)
Gamma hydroxybutyrate
Flunitrazepam (Rhohypnol)
Street names
Rophies Roche
Roofies Roachies
R2 La rocha
Roofenol Rope
Rib
Flunitrazepam (Rhohypnol)
Benzodiazepine
Similar to Valium but 10x more potent
Produced, sold legally in Europe, South
America
Uses
Short-term treatment of insomnia
Sedative hypnotic
Preanesthetic medication
Flunitrazepam (Rhohypnol)
Effects
Disinhibitionand amnesia
Onset within 30 minutes, peak within 2
hours, may persist 8 hours or more
Frequently abused with alcohol or other drugs
Enhances high produced by heroin
Flunitrazepam (Rhohypnol)
Withdrawal
Headache Hallucinations

Anxiety, tension Delirium

Numbness, tingling of Seizures (up to a week

extremities after cessation)
Restlessness, confusion Shock

Loss of identity Cardiovascular

collapse
Gamma hydroxybutyrate
Street names
Cherry meth
Liquid X
Liquid ecstacy

Originally developed as anesthetic

Banned in 1991 because of side effects
Promoted as aphrodisiac
Gamma hydroxybutyrate
Effects
Odorless, nearly tasteless
Tremors
Seizures
Death