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General Kinds of

Poison
Midterm Lecture
Heavy Metals
General Kinds of Poison
 Lewisite Metal
 MOA: Coagulation of protein by binding to -SH
groups
 Signs & Symptoms: “Mee’s Line”, Abnormal
Arsenic Weigh gain, Watery Diarrhea, Milky/rosy
complexion, Garlic odor of breath, Luminous
vomitus, Alopecia, Black line on gums/ bleeding
gums “Raindrop” pattern of Hyperpigmentation &
Hyperkeratosis
 Treatment: BAL/ Dimercaprol
 Sources: Anti-dandruff shampoos, smoke & stink
bamboos, solder
Cadmium  Signs & Symptoms: Osteomalacia, Fractures. Renal
Abnormalities, Gait disturbances
 Treatment: EDTA
• Pharmacokinetics:
 Lead can cross the placenta & pose a potential hazard to the fetus
 Young children have greater degree of absorption of ingested Lead
than adults
 The major route of excretion of Lead is through urine
 Signs & Symptoms:
 Pb encephalopathy

Lead 

Hemolytic Anemia
Abdomical Colic
 Elevated Liver Enzymes
 Pb palsy - wrist/foot drop
 Milky vomitus
 Black stools
 Fanconi-like syndrome

 Treatment: Penicillamine, BAL, EDTA


 MOA: Coagulation of protein by binding to -SH groups
 Signs & Symptoms:
 Acrodinia
 photophobia, anorexia, restlessness, stomatitis, oliguria,
severe diarrhea, pains in arms & legs, pink palms & toes
 Gingivitis
Mercury  Erethism
 Treatment:
 Na Formaldehyde Sulfoximate
 BAL
 Penicillamine
 Chelation w/ Unithiol
 Three Types of Mercury
a) Elemental Mercury
Mercury b) Inorganic Mercury
c) Organic Mercury
 Cause of toxicity: Over ingestion of OTC preparations
 Lethal Dose: 200-300mg/kg
 Toxic Dose: >600mg/kg

Iron  Phases of Toxicity:


I. nausea, vomiting, diarrhea, GI bleeding, hypotension
II. clinical improvement seen 6-24 hours post ingestion
III. metabolic acidosis, renal & hepatic failure, sepsis, pulmonary
edema & death

 Treatment: Deferoxamine/Deferoxime
 MOA: Bind to SH group
 Signs & Symptoms:
 Gastroenteritis
Thallium  Paresthesia
 Alopecia
 Treatment: Prussian blue/ Ferric Ferrocyanide
Drugs of Abuse
 MOA: All bind to opioid receptors Mu, Kappa, Delta
 Signs & Symptoms:
 Triad: Coma Miosis Respiratoy depression
 Treatment:
Opioids  Naloxone
 Naltrexone
 Nalorphine
 Nalmefene
 Activated Charcoal
 MOA: Increases Dopamine activity in the brain
 Treatment:
Amphe  Seizures: Diazepam, Phenytoin
 Psychosis/Agitation: Chlorpromazine, haloperidol,
tamine Diazepam
 Hypertensive crisis: Alpha-blockers, Beta-blockers
 Arrhythmias: Propranolol, Lidocaine
Sedati
Benzodiazepines
ves & • MOA: potentiate neurotransmitters – GABA
• Signs & Symptoms: Drowsiness, Ataxia, Confusion
Hypno • Treatment: Flumazenil

tics
Barbiturates
Sedati • used in induction of anesthesia & for seizures
• Signs & Symptoms:
ves & • Mild: Slurred Speech, Ataxia, Altered mental
status

Hypno • Severe: Comatose with absence of deep


tendon reflexes, Cheyne-Stokes (irregular)
respiration
tics • Treatment: Force Alkaline dieresis (NaHCO3)
Hemodialysis
Sedati Chloral Hydrate
ves & • in vivo via alcohol dehydrogenase
• Trichloroethanol
Hypno • ”Knock-out drops”, similar to barbiturates
• Treatment: Supportive
tics
LSD
• Lysegic Acid Diethylamide
Halluci • MOA: Stimulates serotogenic receptors, Increase
levels of 5-HT5
nogens • Signs & Symptoms: Increase suicidal tendency
and altered mental status
• Treatment: Benzodiazepine
Halluci Mescaline
• peyote cactus (Lophophora williamsii), “buttons”
• one of the first phenylakylamine hallucinogen
nogens identified
Amphetamine derivatives
Ecstacy (MDMA, Methylenedioxymethamphetamine)
• MDA (Methyldioxyamphetamine) –“Love drug”
Halluci • MOA: Acting like false neurotransmitters (act like
catecholamines)

nogens • Toxic dose: 50-150 mg


• Signs & Symptoms: Hypotension, Cardiac arrest,
Death
• Treatment: Force Diuretics, Labetalol,
Nitroprusside, Nifedipine
Methamphetamine
• more substantial than amphetamine
• crystal form ”Crack”, “Speed”, “Yaba”, “Go”, “Ice”,
“Siopao”, “Ubas”, “Batak”, “Bato-Bato”, “Poor
Halluci Man’s Cocaine”
Ephedrine
nogens • Ma huang
• Khat “quat”, “qat”
• from Catha edulis shrub
• Active ingredient in fresh leaves of Khat
 Signs & Symptoms:
 Nystagmus
 Decrease consciousness
Phencyclidine  Acute brain syndrome
(PCP)  Treatment:
 Benzodiazepine
 Diazepam
 NItroprusside
Dimethyl
tryptami  a short acting hallucinogen found in the seeds of
Piptadenia peregrina

ne (DMT)
 Cannabis sativum
 aka Mary Jane, Hash-ish, Hash-oil, Weeds
Marijuana  used a antiemetic for patient undergoing
chemotherapy
 MOA: Increase Dopamine activity
 Treatment:
Cocaine  Seizures: Benzodiazepine
 Psychosis: Neuroleptics
 HPN: Labetalol
 Metabolites: Acetaldehyde, Acetic Acid
 Signs & Symptoms: CNS depression, Acid-base
Ethanol Imbalance, Metabolic Acidosis, Impaired Thermal
Regulation, Hypoglycemia
 Treatment: Thiamine, Disulfiram, Fomepizole
 Acute Nicotine Toxicity: Hypertension, Cardiac
Arrythmia

Nicotine  Management: Anticonvulsant


 Treatment: Activated Charcoal, Gastric Lavage,
Mecamylamine
 Signs & Symptoms: Rigor mortis, Convulsion

Strych  Treatment:
 Diazepam
 Phenobarbital
nine  Neuromuscular Blockers
 Skeletal Muscle Relaxant
Toluene
• Methyl benzene
• “Glue Sniffers”
Volatile Nitrous Oxide
• Anesthetic
Substan • “laughing gas”
• may cause diffusional hypoxia
ces • Hysterical laughing
• blue container in hospital
• Treatment: Ventilation Support, 100% oxygen
Clinical Toxicology
 Signs & Symptoms:
 Mild: Tinnitus
 Severe: Lethargy, Convulsions, coma, Metabolic
Salicyla Acidosis
 Treatment:
tes  Urine Alkalinization with NaHCO3
 Vitamin K1/ fresh frozen plasma
 Hemodialysis or Hemoperfusion
 MOA: Depletion of Glutathione causing Hepatic
necrosis due to its toxic metabolite, NAPQI

Parace  Phases of toxicity:


I. anorexia, diaphoresis

tamol II. asymptomatic


III. abdominal pain, hepatic failure, coma, death
 Treatment: N-Acetylcysteine
 MOA: Inhibition of Vitamin K-related clotting factors
Warfarin  Principal Manifestation: Bleeding
 Treatment: Vitamin K
 Principal Manifestation: Bleeding
Heparin  Treatment: Protamine Sulfate
Chloram  Gray Baby Syndrome: GI disturbance, vomiting,
anorexia, abdominal distention, diarrhea,
hypothermia, hypotension, & cyanosis
phenicol  Treatment: Charcoal Hemoperfusion
Vanco  Red Man or Red Neck Syndrome
 Prevention: Prolonging the infusion to 1-2 hours or
mycin increasing the dosing interval
 Signs & Symptoms:
 Mild: Nausea, vomiting, anorexia, confusion
 Severe: Cardiac dysrhythmias
Digoxin  Treatment:
 Lidocaine or Phenytoin
 Digoxin-specific Fab antibodies
 Potassium Chloride
Succinylcholine & Tubocurarine
 Signs & symptoms: Malignant Hyperthermia and
Muscle Anaphylactic shock
 Treatment:
Relaxants  Epinephrine
 Dantrolene
 Neostigmine
Methy Theophylline
• Signs & Symptoms: Seizures, Cardiac
xanthi Dysrhythmias
• Treatment: Ipecac Syrup, Activated Charcoal,
nes Hemoperfusion & Hemodialysis
 Signs & Symptoms:
 Mild: polyuria, blurred vision, weakness, slurred
speech, Ataxia, tremor & myoclonic jerks
Lithium  Severe: delirium, coma, seizures & hyperthermia
 Treatment: Ipecac Syrup, NA polystyrene sulfonate,
hemodialysis
 Signs & Symptoms:
Tricyclic  Anticholinergic signs & symptoms
 Cardiopulmonary toxicity
Antidep  CNS manifestations

ressants  Treatment:
 Physostigmine
 NaHCO3: DOC for Cardiopulmonary toxicity
(TCAs)  Phenytoin &Benzodiazepine
 Signs & Symptoms:
 Peripheral Neuropathy
 Hepatitis
 Management:
Isoniazid  Pyridoxine is given at a dose of 1mg per mg of
Isoniazid
 Activated Charcoal
 Benzodiazepine
 Treatment: Vitamin B6
Beta-  Signs & Symptoms: Hypotension, Bradycardia, AV
block Bronchospasm

Blockers  Treatment: Glucagon and Epinephrine


Calcium-
 Principal Manifestation: Hypotension
Channel  Treatment: Calcium Chloride and Glucagon

Blockers
 Signs & Symptoms:
 Cardiac Irritability
 Dysrhythmia
 Peripheral Weakness
 Treatment:

Potassium  Calcium Chloride


 NaHCO3
 Glucose
 Insulin
 Cation exchange resin: SPS(Sodium polystyrene
Sulfonate)
 Hemodialysis
End.

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