Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
158 Cards in this Set
- Front
- Back
|
What is the primary determinant of toxicity?
|
Dose, Dose, Dose!
time also matters, accumulation also think: is it an acute exposure or a chronic exposure? |
|
|
What is toxicology
|
A subset of pharmacology that focuses on the detection, properties, effects and regulations of toxic substances and poisions.
|
|
|
What's the difference between a hazard and a risk?
|
Hazard is the potential for harm
Risk is the probability of producing harm |
|
|
Who said, "all substances are poisons and there is none that is not a poision?"
|
Paracelsus
|
|
|
Who said "The right dose differentiates a poision and a remedy"
|
Paracelsus
|
|
|
Who was Paracelsus
|
a Swiss Physician who laid the ground work for modern toxicology. He said that all substances are poisions, and that the right dose differentiates a poison from a remedy.
|
|
|
What are the divisions of modern toxicology?
|
Academic toxicology
Clinicial/Commercial Toxicology Environmental Toxicology Governmental Toxicology Forensic Toxicology |
|
|
Define the TI
|
TI = Therapeutic Index is TD50/ED50
The larger the number the safer the drug |
|
|
Define Acute Toxicity
|
defines intrinsic toxicity - with a single dose within 24 hours
|
|
|
TLV?
|
Threshold limit value -
Concentration below which there is no expected untoward effect over a period of 8 hrs.day, 5 days/wk |
|
|
NOEL?
|
No observable effect level
|
|
|
ADI
|
Allowable daily intake
ADI = NOEL/x x is some safety factor |
|
|
STEL
|
Short term exposure level
4X a day with the average being equal to the TLV |
|
|
ALD
|
Average Lethal Dose - estimated from accidental deaths in humans
|
|
|
Toxicon
|
Toxic principle of a given chemical entitiy
|
|
|
What workplace standard is used to assess exposure to toxic substances?
|
TLV - Threshold Limit Value - the concentration below which there is no expected utowad effect over a period of 8 hours/day, 5 days/wk
|
|
|
What are the steps in poisioning management?
|
1. ABCs - support vital functions
2. ID drug poisioning is the problem 3. Reduce the amount of drug in the body |
|
|
Define nonselectivity vs. selectivity
|
Most toxins are nonselective in their actions
|
|
|
What is a general treatment for a comatose patient?
|
If in a coma, give glucose, insulin, and naloxone ... in case the patient is a (1) diabetic (2) drug addict
|
|
|
How do you ID a poision?
|
Identify poision by
(1) Patient History (2) Laboratory tests (urine or blood) (3) Comparison of drugs or chemicals with known toxicology standards |
|
|
What three types of sample types can be used to ID a poision?
|
(1) Urine
(2) Blood - can tell you the concentration so that you can predict the health effects (3) Gastric contents - will tell you if you need gastric lavage. |
|
|
What types of drugs can be identified using a urine test?
What sort of urine tests do you use? |
Marijuana, Cocaine, amphetamines barbiturates, etc ...
Tests - immunoassay (EMIT, ELISA)& TLC Urine/Blood tests - HPLC & GCMS |
|
|
In a poisioning case, how can you remove the drug?
|
(1) Induce emesis
(2) Gastric lavage (3) Diuresis (4) Alteration of pH (5) Dilution of water (6) Demulcents (smooth mucuous membranes and coats stomach) (7) Hemodialysis |
|
|
What are contraindications for emesis ?
|
(1) petroleum hydrocarbon solvent - when it gets up chucked it can cause chemical pneumonitis
(2) Comatose patient (3) Seizing patient (4) Caustic acid or alkali agent |
|
|
What's the rule about giving activated characol and inducing emesis?
|
Give the activated characol first, becasue if you give it second, it will bind the ipecac and not the toxin
|
|
|
When is activated characol contraindicated?
|
With petroleum distilates and with caustic agents
|
|
|
Tell me about activated characol/cathartics
|
Activated characol binds the toxins, cathartics flush it out of your system.
|
|
|
Antidotal treatment for heavy metal poisioning?
|
Chelators
BAL - British Anti-Lewisite EDTA complexes with the metals making them inert |
|
|
What are the different types of antidotal treatments?
|
(1) Complexation
(2) Enhance the metabolic conversion to a safer form (3) Inhibition of metabolic conversion to the toxic form (4) accelerating the rate of excretion (5) Competition for essential receptors (6) Repair or Bypass effect of poision (7) Blockade of receptors responsible for the toxic effect |
|
|
Antidotal treatment heavy metals
|
Chelators
BAL - British Anti-Lewisite EDTA Complexes with the toxin making it inert |
|
|
Antidotal treatment for heparin
|
Protamine - a base binds to the acidic heparin to terminate its action and cause it to be excreted by glomerular filtration
|
|
|
Antidotal treatment for botulinum toxin Ald
|
abcS, gastric lavage, emesis, activated characol, anti-toxin
|
|
|
Antidotal treatment for organophosphate poisioning
|
pralidoxime is a nucleophilic reagent that ties up the organophosphates and permits its excretion
|
|
|
Antidotal treatment for cyanide poisioning
|
(1) Give amyl nirtrates and na nitrite with O2
(2) Give whole blood to convert hemoglobin to methemeglobin |
|
|
Give an example of antidotal treatment:
Conversion of toxin to a less toxic form |
Rhodanese converts CN --> SCN
note: Rhodanese needs a sulfur source to convert CN --> SCN |
|
|
Give an example of antidotal treatment:
Inhibit conversion of compound to toxic form |
Ethanol out competes methanol, which causes it to not be converted to a toxin by alcohol dehydrogenase
|
|
|
Tell me about CO
|
CO is found in cigarette smoke but not in natural gas
CO has a 210X greater affinity for Hb than for O2 |
|
|
What is an important symptom of CO poisioning? At what concentration are these symptoms seen?
|
Cherry red appearance at 40 - 60% CO concentration
|
|
|
Treatment for CO poisioning?
|
Artificial respiration with pure O2 to promote displacement of CO
competition for essential receptors |
|
|
Treatment for Opiate overdose?
What type of mechanism? |
Naloxone or Naltrexone
competition for essential receptors |
|
|
Treatment for coumadin overdose
What type of mechanism? |
Vitamin K and give whole blood
competition for essential receptors |
|
|
Treatment for tubocurare/ pancuronium?
What type of mechanism? |
Cholinesterase Inhibitors
competition for essential receptors |
|
|
Treatment of Nitrites/sulfa drugs?
What type of mechanism? |
Methylene blue causes a direct reduction of methhemoglobin back to hemoglobin
Repair or bypass effect of poision |
|
|
Treatment for digitalis?
Type of mechanism |
Give Digibin!
Type: Repair or bypass effect of poision |
|
|
Treatment for 5-FU overdose
|
Give thymidine
Type: Repair or bypass effect of poision |
|
|
Examples of repair or bypass effect of poision as treatment?
|
1) 5-FU overdose
2) Digitalis 3) Nitrites/sulfa drugs |
|
|
Examples of competition for essential receptors mechanism of treatment
|
1) Tubocurare/pancuronium
2) Coumadin 3) Opiates |
|
|
Treatment for anticholinesterase overdose?
Type of mechanism? |
Give atropine
Type: blockade of receptors responsible for toxic effects |
|
|
Acetaminophen
Toxicity Mechanism |
centrilobular liver necrosis.
Mechanism of Action: Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents, which then are eliminated in the urine. In acute overdose or when maximum daily dose is exceeded over a prolonged period, the normal pathways of metabolism become saturated. Excess acetaminophen is then metabolized in the liver via the mixed function oxidase P450 system to a toxic metabolite. Under conditions of excessive metabolite formation or reduced glutathione stores, the reactive metabolite is free to covalently bind to vital proteins and the lipid bilayer of hepatocytes; this results in hepatocellular death and subsequent centrilobular liver necrosis. |
|
|
nausea & vomiting, malaise; right upper quadrant abdominal pain & rising liver enzymes after 3-4 days: hepatic dysfunction with jaundice, possible death;
|
Acetamin overdose!
Treatment: (1) N-acetylcysteine (2) Activated Charcol (3) Supportive therapy |
|
|
Amphetamines
Toxicity Mechanism |
Mechanism of Action: CNS and peripheral stimulant. Cause the release of catecholamines (dopamine, norepinephrine & serotonin) from nerve terminals. The signs & symptoms of amphetamine overdose are generally similar to those of cocaine; however, while effects of cocaine last for 10-20 minutes, the duration of amphetamine action is much longer, lasting as long as 10-12 hours.
|
|
|
Symptoms:agitation & hyperactivity, euphoria, chest pain, dry mouth,hyperthermia, nausea & vomiting, mydriasis, anorexia
|
Amphetamine overdose
Treatment: sedation and observation, Use benzodiazepine sedation (nonspecific sympatholysis) to initially manage hypertension Aggressively cool hyperthermic patients |
|
|
Toxicon: Anticholinergics (antimuscarinics)MOA
|
Mechanism of Action: block muscarinic receptors in the CNS and peripheral nervous system.
|
|
|
Symptoms: flushing, dry skin, mydriasis, loss of accommodation, altered mental status, and fever,
|
Anticholinergics (antimuscarinics) overdose
Treatment:The antidote for anticholinergic toxicity is physostigmine salicylate. Physostigmine is the only reversible acetylcholinesterase inhibitor capable of directly antagonizing the CNS manifestations of anticholinergic toxicity; GI decontamination with activated charcoal Manage seizures with benzodiazepines, preferably diazepam or lorazepam. |
|
|
Toxicon: Arsenic MOA
|
Mechanism of Action: Inorganic forms of arsenic are more toxic than organic forms. Very few organ systems escape the toxic effects of arsenic. Trivalent inorganic arsenic inhibits pyruvate dehydrogenase (via binding to sulfhydryl groups), resulting in decreased citric acid cycle activity, and decreased production of cellular ATP. Trivalent arsenic inhibits numerous other cellular enzymes through sulfhydryl group binding. Trivalent arsenic inhibits cellular glucose uptake, gluconeogenesis, fatty acid oxidation, and further production of acetyl CoA; it also blocks the production of glutathione, which prevents cellular oxidative damage.
|
|
|
garlic smell, vomiting and severe diarrhea (watery & bloody)
|
Acute arsenic poisioning
Treatment: Treatment: Dimercaprol (BAL in oil) |
|
|
What do we use Dimercaprol (BAL in oil) for?
|
Arsenic poisioning
|
|
|
whitish lines (Mees lines) that look much like traumatic injuries are found on the fingernails, peripheral neuorpathy & dermal hyperpigmentation/ depigmentation (salt/pepper) of the skin,
|
Chronic Arsenic exposure
Treatment: Dimercaprol (BAL) |
|
|
What's the difference in symptoms between acute arsenic poisioning and chronic arsenic poisioning?
|
Symptoms:
Acute exposure: garlic smell on the breath & tissue fluids, acute distress, dehydration (often), choleralike gastrointestinal symptoms of vomiting and severe diarrhea (watery & bloody) and hypovolemic shock. Chronic exposure: whitish lines (Mees lines) that look much like traumatic injuries are found on the fingernails, peripheral neuorpathy & dermal hyperpigmentation/ depigmentation (salt/pepper) of the skin, scaly palms, hepatic & renal damage, prolongation of the QT, cardiac arrhythmias & ventricular fibrillation. Microcytic hyprochromic anemia is also common with all heavy metal intoxications. |
|
|
physostigmine salicylate
is an antidote for what? |
Antimuscarinic overdose
|
|
|
N-acetylcysteine is an antidote for what?
|
Acetaminophen overdose.
|
|
|
Toxicon: Barbiturates MOA
|
Mechanism of Action: .Barbiturates bind to specific sites on gamma-aminobutyric acid (GABA)-sensitive ion channels found in the central nervous system (CNS), where they allow an influx of chloride into cell membranes and, subsequently, hyperpolarize the postsynaptic neuron.
|
|
|
lethargy, coma, hypothermia, respiratory depression, hypotension
|
Toxicon: Barbiturates
Treatment: ABCs. Activated charcoal, sodium bicarbonate, Hemodialysis and hemoperfusion |
|
|
Toxicon: Benzodiazepines MOA
|
Mechanism of Action: potentiates the activity of GABA. In the CNS this results in sedation, striated muscle relaxation, anxiolysis, and anticonvulsant effects. Stimulation of peripheral nervous system (PNS) GABA receptors may cause decreased cardiac contractility, vasodilation, and enhanced perfusion.
|
|
|
Symptoms: drowsiness, confusion, weakness, amnesia,
|
Toxicon: Benzodiazepines
Treatment: Flumazenil is the DOC to reverse effects of benzodiazepines. ABCs. Single-dose activated charcoal |
|
|
Flumazenil is the DOC to reverse effects of
|
benzodiazepines overdose
|
|
|
Toxicon: Carbon monoxide (CO) MOA
|
Mechanism of Action: CO toxicity causes impaired oxygen delivery and utilization at the cellular level. CO affects several different sites within the body but has its most profound impact on the organs with the highest oxygen requirement (eg, brain, heart). Toxicity primarily results from cellular hypoxia caused by impedance of oxygen delivery. CO reversibly binds hemoglobin, resulting in relative anemia. Because it binds hemoglobin 230-270 times more avidly than oxygen, even small concentrations can result in significant levels of carboxyhemoglobin (HbCO).
|
|
|
Symptoms: flulike symptoms, dyspnea on exertion, confusion, lethargy, dizziness,
|
Toxicon: Carbon monoxide (CO)
Treatment: 100% oxygen or hyperbaric oxygen. |
|
|
Treatment: 100% oxygen or hyperbaric oxygen.
|
CO poisioning
|
|
|
Toxicon: Caustic agents (acid or base) MOA
|
Mechanism of Action: Alkaline ingestions cause tissue injury by liquefactive necrosis (saponification of fats and solubilization of proteins). The hydroxide ion of the base reacts with tissue collagen and causes it to swell and shorten. Small vessel thrombosis and heat production occurs. Acid ingestions cause tissue injury by coagulation necrosis (desiccation or denaturation of superficial tissue proteins).
|
|
|
Symptoms:Oropharyngeal burns, dyspnea & impending airway obstruction, drooling, nausea & vomiting
|
Toxicon: Caustic agents (acid or base)
Treatment: gastric lavage. DO NOT ADMINISTER EMETICS, If within 30 min of ingestion, try dilution: tap water, Antibiotics, H-2 receptor antagonists, Glucocorticoids |
|
|
DO NOT ADMINISTER EMETICS, what toxicon am I?
|
Toxicon: Caustic agents (acid or base)
|
|
|
Toxicon: Cocaine MOA
|
Mechanism of Action: CNS stimulant (blocks the reuptake of catecholamines:5-HT, DA, NorEpi); Na and K channel blocker; commonly coadministered with ethanol to create cocaethylene which has a longer half-life
|
|
|
Symptoms: hypertension, psychosis & the sensation of something crawling on the skin or itchy skin), seizures, hyperthermia, hypertension, tachycardia, dilated pupils (mydriasis). tachydysrhythmias.
|
Toxicon: Cocaine
Treatment: Establish ABC's, benzodiazepines to manage seizures. sodium bicarbonate to manage acidosis. Treat hyperthermia, the (non-lethal) acute effects of cocaine are generally short-lived |
|
|
Toxicon: Cyanide MOA
|
Mechanism of toxicity: Cyanide affects virtually all body tissues, attaching itself to ubiquitous metalloenzymes and rendering them inactive. Its principal toxicity probably results from inactivation of cytochrome oxidase (cytochrome aa3) and, thus, cellular respiration, even in the presence of adequate oxygen stores. Consequently, the tissues with the highest oxygen requirements (eg, brain, heart, liver) are the most profoundly affected by acute cyanide poisoning. Cyanide cabinduce fatality in seconds to minutes following inhalation or intravenous injection, in minutes following ingestion of soluble salts, or minutes (hydrogen cyanide) to several hours (cyanogens) after skin absorption.
|
|
|
Symptoms: bitter almond odor on breath, bitter taste, burning throat, lock jaw, convulsions, coma, respiratory failure.
|
Toxicon: Cyanide MOA
Antidote: ABC's, amyl nitrite (inhaled), sodium nitrite (i.v.) , Sodium thiosulfate |
|
|
Toxicon: Digoxin MOA
|
Mechanism of Toxicity: inhibits Na/K ATPase; cardiac arrhythmias (delayed after-depolarizations w/ abnormal automaticity, depolarization & conduction block, 1st - 3rd degree AV node conduction block, enhanced vagal tone); CNS effects
|
|
|
Symptoms: GI disturbances, cardiac arrhythmias & ECG changes, neurological, visual disturbances
|
Toxicon: Digoxin
Antidote/Treatment: Digoxin Fab fragments (Digibind) Other treatments: oxygen, cardiac monitoring, i.v. access, check electrolyte levels & correct any imbalances. hypokalemia which will increase digitalis toxicity Give atropine for unstable bradyarrhythmias , lidocaine for ventricular arrhythmias Treat any hyperkalemia |
|
|
Symptoms: odor of hydrocarbons, mild burning of the mouth, coughing & respiratory distress, lethargy & depressed sensorium, chemical pneumonitis;
|
Toxicon: Hydrocarbons
Treatment: Management for HC ingestion is supportive. |
|
|
Toxicon: Lead MOA
|
Mechanism of Action: heavy metals bind to sulfhydryl groups in proteins, resulting in alterations in enzymatic activity. Nearly all organ systems are involved, but the nervous system, GI, hematopoietic, renal & cardiovascular systems are most commonly affected the most.
|
|
|
Symptoms: encephalopathy with seizures, GI complaints, Anemia. Lead line,
|
Toxicon: Lead
Treatment: ABCs, EDTA |
|
|
Toxicon: LSD (lysergic acid dieethylamide) MOA
|
Mechanism of Action: interacts with several different serotonin receptor subtypes (agonist at 5-HT1A & 5-HT1C ) and antagonist at 5-HT2 (the later is believed to be not important for producing hallucinations).
|
|
|
Symptoms: disoriented, mydriasis, tachycardia, mild hypertension & tachypnea, tremor.
|
Toxicon: LSD (lysergic acid dieethylamide)
Treatment: supportive care & benzodiazepines (diazepam) to decrease agitation, haloperidol for acute psychosis. |
|
|
Toxicon: Marijuana (cannabis, hashish) MOA
|
Mechanism of Action: the active ingredient is delta-9 tetrahydrocannabinol (THC) which binds to CB1 and CB2 receptors in the brain.
|
|
|
Symptoms: euphoria, relaxation, sense of slowing of the passage of time, the "munchies"). Dysphoric effects, antinausea
|
Toxicon: Marijuana (cannabis, hashish)
Treatment: supportive care. |
|
|
Toxicon: Mercury MOA
|
Mechanism of Action: heavy metals bind to sulfhydryl groups in proteins, resulting in alterations in enzymatic activity.
|
|
|
Symptoms: (irritability), tremors, pink discoloration of the hands & feet, Gingivitis,
|
Toxicon: Mercury
Treatment: ABCs. activated charcoal. administer chelation therapy (BAL) |
|
|
Toxicon: Methanol MOA
|
Mechanism of Action: A CNS depressant, methanol is potentially toxic in amounts as small as a single mouthful. When metabolized by hepatic alcohol and aldehyde dehydrogenase, methanol forms formaldehyde and formic acid, both of which are toxic. The eyes, CNS, and GI tract are affected. Formic acid is the primary toxin that accounts for the majority of the anion gap, metabolic acidosis, and ocular toxicity. Lactic acid also contributes to the anion gap. Formic acid inhibits cytochrome oxidase in the fundus of the eye. Swelling of axons in the optic disc and edema result in visual impairment. Formaldehyde has a short half-life, lasting only minutes. Formic acid is metabolized much more slowly, and it bioaccumulates with significant methanol ingestion.
|
|
|
Symptoms: lethargy, confusion, misty, or snowstorm-like visual disturbances, blindness, coma, seizures,
|
Toxicon: Methanol
Treatment: Dialysis, sodium bicarbonate, folic acid (leucovorin), ethanol infusion |
|
|
Toxicon: Methaqualone MOA
|
Mechanism of Action: a non-barbiturate sedative hypnotic, stimuates the actions of GABA.
|
|
|
Symptoms: resembles barbiturate poisoning. Has more pronounced motor problems (e.g. ataxia), evere muscular hypertonicity and seizures.
|
Toxicon: Methaqualone (quaalude)
Treatment: no diuresis. Diazepam for severe tonicity or seizures (strongly consider phenytoin as an anticonvulsant because barbiturates potentiate the effect of methaqualone). |
|
|
Toxicon: Morphine & similar narcotics MOA
|
Mechanism of Action: opioid receptor agonist
|
|
|
Symptoms: triad of CNS depression, respiratory depression, and pinpoint pupils (miosis) Hypotension & hypothermia. respiratory compromise.
|
Toxicon: Morphine & similar narcotics
Antidote/Treatment: Administer naloxone |
|
|
Toxicon:Organophosphate & carbamate (anticholinesterases)
|
Mechanism of Action: Organophosphates irreversibly bind to cholinesterase, causing the phosphorylation and inactivation of acetylcholinesterase. Carbamate poisoning exhibits a similar clinical picture to organophosphate toxicity. However, unlike organophosphates, carbamate compounds temporarily bind cholinesterase for approximately 6 hours with no permanent damage. Carbamates have poor CNS penetration and cause minimal CNS symptoms.
|
|
|
Symptoms: mental confusion, fasiculations, miosis, bronchospasm, weakness, excessive secretions, nausea, vomiting, and diarrhea (remember: SLUDE). The condition may progress to seizure, coma, paralysis, respiratory failure, and fatality.
|
Toxicon:Organophosphate & carbamate (anticholinesterases)
Antidote/Treatment: atropine, oxygen, pralidoxime |
|
|
Toxicon: Oxalate plant poisoning MOA
|
Mechanism of Action: Nonsoluble calcium oxalate crystals are found in plant stems, roots, and leaves. These needlelike crystals produce pain and edema when they contact lips, tongue, oral mucosa, conjunctiva, or skin. Edema primarily is due to direct trauma from the needlelike crystals and, to a lesser extent, by other plant toxins (eg, bradykinins, enzymes).
|
|
|
Symptoms: (typical of a contact dermatitis, superficial necrosis developing days after initial contact.
|
Toxicon: Oxalate plant poisoning
Treatment: copious water irrigation. Acetaminophen for pain control. Antihistamines (diphenhydramine). |
|
|
Toxicon: Phencyclidine (PCP, angel dust) MOA
|
Mechanism of Action: a NMDA (Glutamate) receptor antagonist. It is primarily metabolized in the liver and undergoes significant enterohepatic recirculation. Clinical effects occur within minutes and can last several hours.
|
|
|
Symptoms: Horizontal, vertical, or rotary nystagmus, blank stare, amnesia, analgesia, combativeness & paranoid behavior, catatonic posturing, hyperreflexia, muscle rigidity, dystonia, hallucinations, coma .
|
Treatment: ABCs, IV hydration and sedation, benzodiazepines (diazepam), (haloperidol), Activated charcoal, Physical and chemical restraints may be necessary.
|
|
|
Toxicon: Phencyclidine (PCP, angel dust) MOA
|
Mechanism of Action: a NMDA (Glutamate) receptor antagonist. It is primarily metabolized in the liver and undergoes significant enterohepatic recirculation. Clinical effects occur within minutes and can last several hours.
|
|
|
Toxicon: Phenothiazines MOA
|
Mechanism of Action: "Anti-transmitter" actions: block histamine, serotonin, norepinephrine and dopamine receptors. Block of alpha-adrenergic receptors.
|
|
|
Symptoms: drowsiness, tremor & rigidity, orthostatic hypotension, and hypothermia (poikliothermia),
|
Toxicon: Phenothiazines
Treatment: gastric lavage, Activated charcoal |
|
|
Toxicon: Phenothiazines MOA
|
Mechanism of Action: "Anti-transmitter" actions: block histamine, serotonin, norepinephrine and dopamine receptors. Block of alpha-adrenergic receptors.
|
|
|
Symptoms: drowsiness, tremor & rigidity, orthostatic hypotension, and hypothermia (poikliothermia),
|
Toxicon: Phenothiazines
Treatment: gastric lavage, Activated charcoal |
|
|
Toxicon: Phenytoin MOA
|
Mechanism of Action: sodium channel blocker, decreases neuronal excitability.
|
|
|
Symptoms: gingival hyperplasia, hirsutism (excessive hairiness), rashes, acne.
|
Toxicon: Phenytoin
Treatment: ABCs. Activated charcoal. Hemodialysis or hemoperfusion are ineffective for enhancing elimination. Benzodiazepine for seizures. |
|
|
Toxicon: Salicylates MOA
|
Mechanism of Action: Salicylates cause an uncoupling of oxidative phosphorylation. Catabolism occurs secondary to the inhibition of ATP-dependent reactions with the following results: increased oxygen consumption,increased carbon dioxide production, accelerated activity of the glycolytic and lipolytic pathways, depletion of hepatic glycogen,hyperpyrexia.
|
|
|
Symptoms: hyperventilation, respiratory alkalosis, A severe metabolic (ketolactic) acidosis, Excretion of hydrogen ions produces acidic urine. Ototoxicity, tinnitus, tachycardia, CNS depression, seizures, nausea & vomiting, GI hemorrhage, prolonged bleeding time, dehydration.
|
Treatment: ABCs. Gastric lavage, activated charcoal, Hemodialysis, Sodium bicarbonate , Monitor glucose levels closely.
|
|
|
Toxicon: Theophylline MOA
|
Mechanism of Action: Theophylline affects the cardiovascular (CV), neurological, GI, and metabolic systems. Hypokalemia, hyperglycemia, hypercalcemia, hypophosphatemia, and acidosis commonly occur after an acute overdose. Medication, diet, and underlying diseases can alter its narrow therapeutic window. Adverse effects can be evident at therapeutic serum levels.
|
|
|
Symptoms: nausea, sinus tachycardia, tremors, seizures, hypotension, and significant dysrhythmias.
|
Toxicon:Theophylline
Treatment: ABCs. doses of activated charcoal, bowel irrigation. Propranolol or other beta blockers can block a beta-mediated sinus tachycardia & hypotension. Phenobarbital is prefered over phenytoin for treatment of convulsions; most anticonvulsants are ineffective. Hemodialysis |
|
|
Toxicon: Tricyclic antidepressants MOA
|
Mechanism of Action: TCAs affect the cardiovascular, central nervous, pulmonary, and gastrointestinal systems. The toxic effects on the myocardium are related to the blocking of fast sodium channels, which involves the same mechanism as type IA antiarrhythmics (eg, quinidine). CNS toxicity results from the anticholinergic effects and direct inhibition of biogenic amine reuptake.
|
|
|
Symptoms: tachycardia, hypotension, confusion or hallucinations, mydriasis, dry mucous membranes and skin, decreased bowel sounds, urinary retention, seizures, QRS prolongation & arrhythmias.
|
Toxicon: Tricyclic antidepressants
Antidote/Treatment: ABCs, activated charcoal to prevent further absorption, sodium bicarbonate, benzodiazepines (lorazepam) for seizures. |
|
|
the number one cause of fatality from drug ingestion.
|
Notes: In the US: Approximately 500,000 cases of TCA toxicity per year are reported.
Fatality before reaching a healthcare facility occurs in approximately 70% of patients attempting suicide with TCAs. Tricyclic antidepressants are the number one cause of fatality from drug ingestion. Only 2-3% of TCA overdoses that reach a health care facility result in death. |
|
|
Drug: EDTA (ethylene diamine tetra acetic acid) MOA
|
Drug Class: Heavy Metal Chelator
Mechanism of Action: used as a disodium calcium salt. Forms a soluble heavy metal chelate in the blood which is excreted through the urine. |
|
|
Indications: chelator for lead (Pb) & cadmium (Cd). Used in combination with BAL when lead levels are >70 ug/dl
|
Drug: EDTA (ethylene diamine tetra acetic acid)
|
|
|
primary drug of choice for methyl mercury & copper poisoning
|
N-acetylpenicillamine (NAP)
|
|
|
secondary agent for treatment of copper & arsenic poisoning.
|
Drug: Penicillamine
|
|
|
Drug: Penicillamine
|
Drug Class: Heavy Metal Chelator
Mechanism of Action: chelating agent recommended for the removal of excess copper (e.g.in patients with Wilson's disease). |
|
|
N-acetylpenicillamine (NAP)
|
Drug Class: Heavy Metal Chelator
Mechanism of Action: chelating agent recommended for the removal of excess copper (e.g.in patients with Wilson's disease). |
|
|
Drug: Succimer (Chemet ® ) MOA
|
Drug Class: Heavy Metal Chelator
Mechanism of Action: metal chelating agent |
|
|
Indications: Secondary drug to BAL & EDTA for use in the treatment of acute lead poisoning, to remove excess lead from the body, especially in small children. Used when lead concentration is > 45 ug/dl.
|
Drug: Succimer (Chemet ® )
|
|
|
Drug: Dimercaprol (BAL in oil) MOA
|
Drug Class: Heavy Metal Chleator
Mechanism of Action: Forms a chelate by binding sulfhydryl groups with arsenic, mercury, lead, and gold, thus increasing both urinary and fecal excretion of the metals. |
|
|
Indications: Acute arsenic, mercury, and gold poisoning. With EDTA in acute lead poisoning. Not effective for chronic mercury poisoning.
|
Drug: Dimercaprol (BAL in oil)
|
|
|
Drug: Deferoxamine (Desferal ® )MOA
|
Drug Class: Iron chelator
Mechanism of Action: an iron-chelating agent. Desferal chelates iron by forming a stable complex that prevents the iron from entering into further chemical reactions. It readily chelates iron from ferritin and hemosiderin but not readily from transferrin; it does not combine with the iron from cytochromes and hemoglobin. Desferal does not cause any demonstrable increase in the excretion of electrolytes or trace metals. |
|
|
Indications: --------- is indicated for the treatment of acute iron intoxication and of chronic iron overload due to transfusion-dependent anemias.
|
Deferoxamine (Desferal ®
|
|
|
Activated characol is not used as treatment
|
Arsenic
Amphetamines |
|
|
Flumazenil DOC for ----
|
Benzodiazepines
|
|
|
Emesis is NOT indicated
|
Benzodiazepines
Barbiturates Caustic agents (acids or bases) |
|
|
what's the source of caustic agents?
|
ingest automotive battery liquid ingestion
toliet bowl cleaning product rust removal product ingestion metal cleaning product ingestion cement cleaning product ingestion drain cleaning product ingestion |
|
|
what's the difference in mechanism between ingesting a caustic acid vs. ingesting a caustic base?
|
(1) BASE - alkaline ingestion causes tissue injury by liquefactive necrosis (saponification of fats and solubilization of proteins). OH ion of base reacts with tissue collagen and causes it to swell and shorten
(2) Acid ingestion causes tissue injury by coagulation necrosis (desiccation or denaturation of superificial tissue proteins) |
|
|
What do you NOT do if you are treating a child who ingested lots of toliet bowl cleaner?
|
Do not administer emetics because you may subject their oropharyngeal pathway to futher damage.
DO: Do gastric lavage, diluation with water, give antibiotics if suspected perforations, and give H2 receptor antagonists to reduce exposure of injured tissues to acid secretion, glucocorticoids to prevent esophageal strictures. |
|
|
Use benzodiazepines to treat seizure in pts with which overdoses?
|
1) Amphetamine (manage hypertension)
2) Anticholinergics 3) Cocaine overdose 4) organophosphate poisioning 5) PCP or Angel dust |
|
|
Treatment for lead poisioning?
|
ABCS, EDTA
|
|
|
EDTA is treatment for what type of poisioning?
|
Lead poisioning
|
|
|
What's the difference in symptoms between mercury poisioning and lead poisioing? (Both heavy metals that bind the sulfhydryl groups of proteins altering their function)
|
mercury poisioning: irritability, tremors, pink discoloration of the hands nad feet, gingivitis
lead poisioning: encephalopathy with seizures, GI complaints, anemia, lead line in gums (black line in gums) |
|
|
What's the difference in treatment between lead poisioning and mercury poisioning?
|
mercury - give BAL, GI decontamination with activated charcol, control ABCs
Lead - give EDTA, control ABCs |
|
|
What's the role of folic acid in treatment of patients overdosing on methanol?
|
Folic acid (leucovorin) potentiates the conversion of formic acid to CO2 and H20, which helps to get the formic acid out of the body.
|
|
|
What's the difference in methaqualone overdose and barbituate overdose?
|
About the same, only
Methaqualone has more pronounced motor problems (ataxia - failure of muscle coordination) can lead to severe musclular hypertonicity and seizures |
|
|
What can you use to treat organophosphate poisioning but not carbamate poisioning?
|
Pralidoxime
|
|
|
Symptom is rotary nystagmus, what did I eat/smoke/whatever?
|
Phencyclidine (PCP)
|
|
|
Source: NSAID
|
Acetaminophen
|
|
|
Source: drugs of abuse
|
Amphetamines
Marijuana Cocaine LSD PCP |
|
|
Source: H1 blockers, plants (jimson weed, nighshades, and non-commercial mushrooms)
|
antimuscarinics
|
|
|
Source: Industrial exposure (metal foundries, glass production, semiconductor industries), rodenticide, contaiminated wine, malicious intent
|
Arsenic
|
|
|
Source: sedative/hypnotic/anesthetic
|
Barbituates
|
|
|
Source: Sedative hypnotic, antiepileptic
|
Benzodiazepines
|
|
|
source: colorless, odorless gas produced by incomplete combustion of organic compounds, malfunctioning exhaust systems, cigarette smoke, improperly vented gas water heaters, kerosene space heaters, characoal grills, hibachis, sterno stoves
|
Carbon monoxide
|
|
|
Source: toliet bowl cleaning products, automotive battery, rust removal product, metal cleaning product, cement cleaning product, drain cleaning product
|
caustic agents (acids or bases)
|
|
|
Source: fumigates & insectisides, smoke inhalation from industrial fires
|
cyanide
|
|
|
source: found in homes and almost every industrial business
|
hydrocarbons
|
|
|
Source: paints & dyes
|
lead
|
|
|
source: vapors, inorganic and organic forms
|
mercury
|
|
|
source: cleaning materials, solvents, paints, varnishes, sterno fuel, fomaldehyde solutions, antifreeze, gasohol, moonshine, windshield washer fluid, duplicating fluids
|
Methanol
|
|
|
Source: sedative hypnotic
|
methaqualone
|
|
|
source: narcotic analgesic
|
morphine
|
|
|
source: pesticides, chemical warfare
|
organophosphates and carbamates
|
|
|
source: caladium, philodendron, calla lily, skunk cabbage, and others
|
oxalate plant poisioning
|
|
|
source: dissociative anesthetic
|
PCP
|
