Drugs and their antidotes (toxicology) Flashcards

1
Q

Opioid

A

Naloxone (Narcan), Nalmefene (Revex), Naltrexon (Revia)

MoA: Naloxone is an opioid antagonist. It competes at three CNS opioid receptors (μ, κ, δ) and leads to reversal of the depressive opioid effects.

IV is best in emergency, rapid onset of action (1-2 minutes.

Because is has no agonist activity, naloxone will not worsen respiratory depression. When administered, patient should be monitored for respiratory rate changes (and opiate withdrawal symptoms) as the goal of therapy is to restore adequate spontaneous respirations. to avoid withdrawal, use the lowest possible dose that maintains proper ventilation.

Patient should be observed for RD after discontinuation of therapy because the half-life of naloxone may be shorter than that of the opioid. If patient is unresponsive to 10mg naloxone, it is doubtful that an opioid is causing the RD.

Use with caution in the physically dependent (can precipitate withdrawal) and those with preexisting cardiovascular disease or those receiving cardiotoxic drugs.

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2
Q

Digoxin, Digitoxin

A

Digoxin immune antibody fragment or Digoxin immune Fab (Digibind, DigiFab)

MoA: Binds digoxin in plasma, promotes redistribution from tissues, and enhances elimination in the urine. Digoxin becomes inactive once bound to Digoxin immune Fab.

Chronic digoxin toxicity typically begins with the nausea/vomiting/diarrhea/fatigue/confusion/blurred vision or diplopia/arrhythmias. Toxicity can be cause by deterioration of renal function, hypokalaemia, or drug interaction.
Acute digoxin toxicity has early symptoms similar to those of chronic but the onset is more abrupt.

Digoxin immune Fab is a monovalent, digoxin-specific, antigen-binding fragment (Fab) that is produced in healthy sleep. Random fact, it should not be used in patients hypersensitive to sheep because Digoxin immune Fab is derived from the antibodies of sheep.

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3
Q

Cyclophosphamide, Ifosfamide

A

Mesna (Mesnex)

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4
Q

Coumadin/Warfarin/Superwarfarins

A

Vitamin K1 (Mephyton, AquaMephyton), Fresh frozen plasma

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5
Q

Heparin

A

Protamine sulfate

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6
Q

Iron

A

Deferoxamine (Desferal)

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7
Q

Arsenic, Gold, Lead

A

Dimercaprol aka British antilewisite (BAL-in-Oil), Succimer (Chemet)

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8
Q

Cyanide

A

Sodium nitrite 3% + Sodium thiosulfate (Cyanide Antidote Kit), Hydroxocobalamin (Cyanokit)

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9
Q

Benzodiazepine

A

Flumazenil (Romazicon)

MoA: It’s a competitive antagonist of the benzodiazepine receptor in the central nervous system.

In suicidal overdose, flumenazil is rarely used because of the risk of potential co-ingestants. It should not be used in other mixed overdoses that can decrease the seizure threshold (i.e. haloperidol, bupropion, lithium). Co-ingestants of tricyclic antidepressants may precipitate ventricular dysrhythmias or seizures.

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10
Q

Atropine, Anticholinergic compounds

A

Physostigmine salicylate (Antilirium)

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11
Q

Acetaminophen

A

Acetylcysteine (Mucomyst 10%/20%, Acetadote 20%)

MoA: supplies glutathione to aid metabolsim of the reactive metabolite. May provide sulfate for acetaminophen metabolism and minimize the formation of free radicals.

For best results, administer <10 hours after overdose. Minimally effective 24 hours after ingestion.

Therapy is determined by obtaining a serum concentration of acetaminophen between 4-24 hours after ingestion and plotting it on the acetaminophen nomogram to determine whether there is a risk for hepatotoxicity.

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12
Q

Doxorubicin

A

Dexrazoxane (Zinecard)

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13
Q

Anticholinesterase-Organophosphates insecticide poisoning or chem-bioterrorism nerve agent poisoning

A

Pralidoxime hcl (Protopam) [with Atropine]

MoA: Pralidoxime is indicated in combination with atropine (to resolve nicotinic [muscle weakness, diaphragmatic weakness, fasciculations, muscle cramps] and central [coma, seizures] cholinergic manifestations).

It is ineffective for organophosphates without anticholinesterase activity! Use in carbamate poisoning is controversial but some sources recommend it in severe cases.

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14
Q

Insulin, β-blocker, CCB

A

Glucagon (GlucaGen), IV Dextrose

also Calcium chloride 10% for CCB

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15
Q

Digitalis toxicity, hypercalcaemia

A

Edetate disodium

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16
Q

Lead

A

Succimer (Chemet), Dimercaprol aka British antilewisite (BAL-in-Oil) Edetate calcium disodium - EDTA (Calcium Disodium Versenate)

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17
Q

Acetylcholine, Cholinergic agent, Carbamates, Organophosphates, (Bradycardia)

A

Atropine

MoA: It’s an anticholinergic agent that competitively inhibits acetylcholine at muscarinic receptors. Little to no effect on nicotinic receptors.

Dosaging varies, but in severe poisoning doses of up to 100mg over a few hours or several weeks may be required.

When large doses of atropine are used, the product should be preservative-free because agents such as benzyl alcohol or chlorobutanol can produce their own toxicity.

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18
Q

Cyanide

A

Hydroxocobalamin

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19
Q

Methotrexate, Trimethorpim, Pyrimethamine

A

LeucovorinCa2+ (Wellcovorin)

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20
Q

Ethylene glycol, methanol

A

Ethanol 10%, Fomepizole (Antizol)

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21
Q

Isoniazid

A

Vitamin B6 - Pyridoxine

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22
Q

Methemoglobinaemia

A

Methylene blue

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23
Q

Salicylate, Tricyclic antidepressants, agents with type 1a antiarrhythmic effects

A

Sodium bicarbonate

24
Q

Emergency Action:

Inhaled poison

A

Immediately get the person to fresh air

Avoid breathing fumes

Open doors and windows wide

25
Q

Emergency Action:

Poison on the skin

A

Remove any contaminated clothing (carefully)

Flood skin with water for at least 15 minutes

26
Q

Emergency Action:

Poison in the eye

A

Remove contact lenses

Flood the eye with large glass of water, 2-3 inches away, repetitively for 15-30 minutes

Do not force eyelid open

27
Q

Emergency Action:

Swallowed poison

A

Give small glassful of water of 2-4 oz immediately (unless they unconscious, having convulsion, or cannot swallow)

Call a poison center for advice about whether other actions are needed

Other considerations:
- avoid wasting time to find an “antidote” at home
- do not use home remedies such as saltwater, mustard powder, raw eggs, H2O2, cooking grease, or gagging
- immediately call 911 or an ambulance if the person is not breathing, has had a seizure, or is unresponsive
for other situations, contact poison center to determine first aid or whether a poisoning emergency exists

28
Q

Non-antidote methods (1/6) - Ipecac syrup

A

Do not give if time since ingestion is believed to be > 1 hour.

Ipecac syrup has questionable effectiveness, and its use is generally avoided. It is used primarily at the preference of the consulting poison center or health care professional. Emesis complicates administration of other oral therapies.

In 2003, the American Academy of Paediatrics recommended that it no longer be used routinely as a home treatment.

Contraindicated in sleepiness, coma, seizures, or ingested caustics, aliphatic hydrocarbons, tricyclic antidepressants, clonidine, CCB’s, β-blockers.

29
Q

Non-antidote methods (2/6) - Activated charcoal

A

Do not give if time since ingestion is believed to be > 1-2 hours.

Activated Charcoal is used to adsorb poisons in an alert or comatose patient. Administer as a slurry by mouth or through lavage tube.

Patients commonly experience emesis or soiling of clothes and furnishings. Activated charcoal is messy, difficult to administer and may remove beneficial drugs with the toxin.

Should not be given is aliphatic hydrocarbons, caustics, heavy metals (sodium, lithium, iron, lead) have been ingested or if patient has absence of bowel sounds.

Advantages include rapid onset, non-specific action for a wide variety of chemicals.

30
Q

Non-antidote methods (3/6) - Cathartics

A

Examples are magnesium citrate, magnesium sulfate, sodium sulfate, sorbitol.

They were previously used as an adjunct to activated charcoal to decrease GI transit time but their efficacy is unproved.

Fluid and electrolyte disturbances are possible with repeated doses.

31
Q

Non-antidote methods (4/6) - Gastric lavage

A

Do not use if time since ingestion is believed to be > 1 hour.

Involves placing a tube into the stomach, via nostril of mouth, and repeatedly washing out the stomach contents with water or saline.

This decontamination method is of questionable effectiveness, particularly after the cut-off window of 1 hour.

32
Q

Non-antidote methods (5/6) - Whole-bowel irrigation

A

Most effective when used if ingestion time is < 2 hours.

This method is used when activated charcoal may be inappropriate (e.g. if iron or lithium was ingested) and the toxin is known to be in the GI tract (i.e. sustained-release drugs or illicit drugs packed in condoms).

Use larger volumes of polethylene glycol electrolyte solutions (e.g. Colyte, Golytely) than amounts conventionally used for bowel preparation.

Do not used this method if the patient has ingested caustics, aliphatic hydrocarbons or when there is an absence of bowel sounds or GI tract obstruction.

This method is very messy because of rectal effluent.

33
Q

Non-antidote methods (6/6) - Haemodialysis

A

A medical procedure to remove fluid and waste products from the blood and to correct electrolyte imbalances. This is accomplished using a machine and a dialyzer, also referred to as an “artificial kidney.”

34
Q

Lithium

A

Whole-bowel irrigation or Haemodialysis

35
Q

Poison Prevention Packaging Act of 1970

The Joint Commission on Accreditation of Healthcare Organizations

A

To prevent young children from opening and ingesting harmful substances.

Poison Prevention Packaging Act of 1970
*Requires the use of safety caps for most drugs, with certain exceptions (birth control, nitroglycerine, anti-arthritis medication).

The Joint Commission on Accreditation of Healthcare Organizations

  • Prevention can be achieved by storing out of the reach of children, using safety caps/safety latches properly, and never putting chemicals in food containers.
  • Maintain and keep an approved stock of antidotes and other emergency drugs in the pharmacy and patient care areas.
  • Maintain authoritative, current antidote information.
  • Keep the phone number of the poison control center readily available in areas outside the pharmacy where drugs are stored.
36
Q

Terrorism and Disaster Preparedness - Biological Threats

The CDC guides health professional on these matters: https://emergency.cdc.gov/

(explosives and weapons are not covered)

A

Bioterrorism is the deliberate use of infectious biological agents to cause illness.

They include smallpox, anthrax, plague (Yersinia pestis), botulism, tularemia, and viral hemorrhagic fevers (e.g. Ebola, Marburg, Lassa, and Machupo).

37
Q

Terrorism and Disaster Preparedness - Chemical Threats

The CDC guides health professional on these matters: https://emergency.cdc.gov/

(explosives and weapons are not covered)

A

Toxic chemicals used in warfare and in a chemical terrorism attack include nerve, blister, or vesicant; blood; choking, lung, or pulmonary; incapacitating; and riot control tear- and vomit-inducing agents.

The CDC also considers as threats several commonly available agents, such as hydrofluoric acid, benzene, and ethylene glycol (antifreeze), and metals such as arsenic, mercury, and thallium, but these agents are not detailed studied in these flashcards.

38
Q

Terrorism and Disaster Preparedness - Radiological Threats

The CDC guides health professional on these matters: https://emergency.cdc.gov/

(explosives and weapons are not covered)

A

Radiological weapons involve nuclear radiation or radioactive materials with various radionucleotides. Radionucleotides can produce topical and systemic effects that may be immediate or delayed, depending on the agent, route of exposure, and extent of exposure.

Medical management of radiological emergencies and terrorist attacks is specific for the radionucleotide.

Guidance on treatment is available from the Radiation Emergency Assistance Center/Training Site (REAC/TS), also check out this link: http://orise.orau.gov/reacts/

Further info:

  • Many individuals near nuclear reactors will maintain a stock of stable iodine tablets in the event of a radioactive accident.
  • The early use of stable iodine, taken as potassium iodide or sodium iodide tablets, can reduce the uptake of radioiodine by the thyroid.
  • Ingestion of stable iodine is of little value for other radionucleotide exposures unless the radioactive constituents are unknown, as in a “dirty bomb”.
  • Calcium and zinc salts of DTPA for IV infusion and aerosol nebulization (Ca-DTPA and Zn-DTPA) are approved (available form the CDC) to treat patients who have been exposed to radionucleotides that may be found in a dirty bomb, such as plutonium, americium, and curium. The drugs form chelates with the radionucleotides that are excreted in the urine.
  • Prussian blue 500mg capsules (available from the CDC) are approved for treatment of patients with exposures to radioactive cesium (Cs-137) and thallium (Tl-201). Prussian blue absorbs the radioactivity that is recirculated in the intestines and thereby enhances its elimination in the stool.
39
Q

Terrorism and Disaster Preparedness - Emergency Preparedness

The CDC guides health professional on these matters: https://emergency.cdc.gov/ and the SNS Program [Strategic National Stockpile (SNS) and CHEMPACK]

A

The CDC advises citizens who believe that they have been exposed to a biological or chemical agent - or believe an intentional biological threat will occur or is occurring - to contact their local health department, local police, or another law enforcement agency (e.g. the FBI - Federal Bureau of Investigation). These agencies will notify the state health department and other response partners, in accordance with a preestablished notification list that channels to the CDC.

The CDC maintains the Strategic National Stockpile (SNS) to ensure availability and rapid deployment of life-saving pharmaceuticals, antidotes, other medical supplies and equipment necessary to counter nerve agents, biological pathogens, and chemical agents. The SNS program stands ready for immediate deployment to any US location in the event of a terrorist attack using biological toxin or chemical agent directed against a civilian population. A limited stock of drugs to treat nerve agents (CHEMPACK) has been deployed to emergency medical services and hospital sites throughout the US and is maintained by the CDC.

Pharmacists should consider volunteering in their communities to assist with emergency preparedness. Roles in mass dispensing and vaccination clinics, are possible opportunities. Contact the local health department or emergency medical services agency.

40
Q

Biological Agent: Smallpox

Cause: variola virus

Spread: aerosol, direct contact (persons or fluid)

A

Clinical features: similar to chickenpox but rash is predominantly further out towards the face and limbs/extremities, especially the palms and soles (less prominence on the torso; as seen with chickenpox) with lesions forming all at once (chickenpox develops in groups of lesions over several days).

Treatment: No specific treatment.

Vaccine: A live virus vaccine of vaccinia virus (Dryvax) is primarily preventive for close contacts, but vaccination within 4 days of exposure may prevent or lessen disease.

41
Q

Biological Agent: Anthrax

Cause: bacillus anthracis

Spread: cutaneous, inhalation, GI (none are contagious) are the three major forms

A

Clinical features: small papules become vesicles within 1-2 days (cutaneous), sore throat/chest discomfort and minimal-productive cough progressing into respiratory failure/shock with meningitis frequently developing (inhalation), severe oropharnygeal/abdominal distress followed by signs of fever/septicaemia/bloody vomit/diarrhea (GI)

Treatment: ciprofloxacin and doxycycline are FDA approved for PEP (postexposure prophylaxis) for children and adults and levofloxacin for adults 18+ years only. Amoxicillin and penicillin may be used in hypersensitivity. Persons at risk of inhalation of anthrax need 60 days of prophylactic ABX.

Vaccine: Anthrax vaccine adsorbed (BioThraxT) given IM is indicated for the active immunization fo the prevention of disease caused by bacillus anthracis in persons between 18-65 years of age at high risk of exposure.

42
Q

Biological Agent: Plague

Cause: yersinia pestis

Spread: pneumonic plague is the most virulent

A

Clinical features: fever, cough, mucopurulent sputum, hemoptysis, chest pain, sever pneumonia symptoms within 1-6 days, septic shock, high mortality can occur within 2-4 days. Y.pepsis cause bubonic plague is less likely to be weaponized.

Treatment: for pneumonic plague - early treatment with streptomycin or gentamicin is advised. Other ABX may also be effective.

Vaccine: no longer manufactured

43
Q

Biological Agent: Botulism

Cause: clostridium botulinum

Spread: foodborne, airborne

A

Clinical features:

Treatment: Antitoxin (most effective within 24 hours of exposure) is maintained and dispensed by the CDC. Most patients recover, often with mechanical ventilation for weeks to months.

Vaccine: No

44
Q

Biological Agent: Tularemia

Cause: francisella tularesis

Spread: most infectious bacteria known

A

Clinical features: acute symmetric descending paralysis in a proximal to distal pattern, with prominent bulbar palsies such as diplopia, dysarthria, dysphonia, and dysphagia that usually presents 12-72 hours postexposure and with respiratory dysfunction from respiratory muscle paralysis or upper aurway obstruction without sensory deficits.

Treatment: Prompt treatment with streptomycin, gentamicin, chloramphenicol, doxycycline, or ciprofloxacin is advised, as is early PEP (postexposure prophylaxis) use of doxycycline or ciprofloxacin.

Vaccine: No

45
Q

Biological Agent: Viral haemorrhagic fevers - VHF (Ebola, Marburg, Lassa, Machupo, Bolivian Haemorrhagic Fever, Rift Valley Fever, Yellow Fever, Omsk Haemorrhagic Fever, Kyasanur Forest Disease)

Cause: filoviruses, arenaviruses, bunyaviruses, flaviviruses

Spread: aerosol, direct contact

A

Clinical features:

  • filoviruses (Ebola and Marburg types) abrupt onset of undifferentiated febrile illness with high fever occurring 2-21 days after exposure. Maculopapular rash, prominent on the trunk develops approx. 5 days later, with progressive bleeding symptoms such as petechiae, ecchymosis, disseminated intravascular coagulation and haemorrhages.
  • arenaviruses (Lassa and multiple New World arenaviruses, including Machupo, which causes Bolivian haemorrhagic fever) symptoms and onset are similar to those of filoviruses, but with a gradual onset of rash, haemorrhagic diathesis, and shock.
  • bunyaviruses (Rift Valley virus) <1% develop haemorrhagic fever.
  • flaviviruses (Yellow Fever, Omsk haemorrhagic fever, Kyansur Forest disease), other VHFs exist but they are not considered a serious bioterrorism risk.

Treatment: No FDA approved antiviral drugs. Maintain fluid/electrolyte balance, circulatory volume, BP and give support.

Vaccine: No vaccines are available

46
Q

Biological Agent: Ricin

Cause: castor beans

Spread:

A

Clinical features: within a few hours, dyspnoea and cough develop with the lungs becoming severely inflamed and filled with fluid. Skin might turn blue from cyanosis or flush red. Ingestion causes internal bleeding of the stomach and intestines. Injection kills the closest muscles and lymph nodes before spreading to other organs.

Treatment: No antidote is available. Death from multiple organ failure within 36-48 hours. If victims survive more than 5 days, survival is likely.

Vaccine: No

47
Q

Chemical Agent (military name): Nerve agents

A

Examples: (G agents and V agents): sarin (GB), soman (GD), tabun (GA), cylohexyl sarin (GF), S-[2-(diisopropylamino)ethyl]-O-ethyl methyl-phosphonothioate (VX)

Clinical Features: These agents are organophosphates that attach to and inhibit acetylcholinesterase at muscarinic and nicotinic receptors, causing cholinergic crisis with miosis; vomiting; diarrhea; excessive bronchial, lacrimal, dermal, nasal, and salivary secretions; bradycardia or tachycardia; skeletal muscle fasciculations; paralysis; seizures; and respiratory failure. They are well absorbed through all routes of exposure. Symptoms occur within minutes after significant exposure and up to 18 hours after liquid exposure.

Treatment: Rapid, thorough decontamination is necessary. Antidotes include atropine to reverse muscarinic symptoms and pralidoxime early to restore acetylcholinesterase before permanent deactivation (aging) of the enzyme. Also give diazepam or lorazepam for seizures.

48
Q

Chemical Agent (military name): Blister agents

A

Examples: Mustards and nitrogen mustards; lewisites; chloroarsines; mustard-lewisite combinations; phosgene oxime (CX)

Clinical Features: Mustards are vesicants that cause blistering of the skin and mucous membranes on contact, damaging skin, eyes, lungs. Damage is immediate, but symptoms can be delayed 2024 hours. Liquids are more likely to cause burns and scarring than are gasses. All forms are absorbed through the skin and distributed systematically. Nitrogen mustards cause bone marrow suppression in 3-5 days. Sulfur mustards have garlic, onion, mustard, or no odour. Nitrogen mustards can smell fishy, musty, soapy, or fruity. Lewisites and chloroarsines are arsenical vesicants that cause immediate pain and damage to the eyes, skin, and respiratory tract, although lesions may take hours to form. After absorption, they cause increased capillary permeability, leading to hypovolaemia, shock, and organ damage. Lewisite smells like geraniums. Mustard-lewisite is lewisite combined with distilled mustard. Phosgene oxime is readily absorbed and causes immediate, painful, corrosive and necrotic tissue damage and has disagreeable odour.

Treatment: Sulfur and nitrogen mustards (thought to be alkylating agents that cross-link DNA strands) have no antidote. Avoiding contact or rapid thorough decontamination is the only means of prevention. Treatment is supportive. Exposure is not usually fatal (sulfur type <5% fatal in WWI). No mustard is found in tissue or blister fluids. British antilewisite is a specific antidote for lewisite, used IM for systemic effects or topically as skin or eye ointment. Chloroarsine treatment is similar, expect atropine sulfate ointment is used for eyes. No antidote exists for phosgene oxime. Rapid decontamination and supportive treatment are used, as for any corrosive agent.

49
Q

Chemical Agent (military name): Blood agents

A

Examples: Arsine (SA); cyanide gases such as hydrogen cyanide (AC) and cyanogen chloride (CK); cyanide solids such as potassium cyanide (KCN) and sodium cyanide (NaCN)

Clinical Features: Arsine is a gas that causes nausea, vomiting, haemolysis, and secondary renal failure in 1-2 hours to 11 days. It has a garlic-like odour. Inhalation of highly concentrated cyanide causes an increased rate and depth of breathing in 15 seconds, convulsions within 30 seconds, cessation of respiration in 2-4 minutes, and cessation of heartbeat in 4-8 minutes. Progress and severity of symptoms after ingestion or inhalation of lower gas concentrations are slower and dose dependent. Cyanide gas may have an odour of bitter almonds or peach kernels (AC), or no odour with irritating, lacrimating properties like riot control agents (CK).

Treatment: Arsines require symptomatic management of haemolysis, normally without chelation.
Cyanides bind to cytochrome oxidase. Two antidotes are available. Cyanide Antidote Kit (sodium nitrite, a methemoglobin-forming agent, binds cyanide and a sulfur donor to convert it to excretable sodium thio-cyanate/sulfate) and CyanoKit (hydroxocobalamin combines with cyanide to form nontoxic cyanocobalamin). Fresh air and oxygen are essential as supportive treatment.

50
Q

Chemical Agent (military name): Choking and Pulmonary agents

A

Examples: Phosgene (CG), diphosgene (DP); also ammonia, chlorine (Cl), hydrogen chloride (HCl), nitrogen oxide (NO), perfluoro-isobutylene (PFIB), *others

Clinical Features: Phosgene gas causes eye, nose, throat, and pulmonary irritation, with serious pulmonary injury and oedema delayed up to 48 hours as it hydrolyses to hydrochloric acid (HCl) in moist conditions. It has a new-mown-hay odour. Phosgene is the prototype agent in the group. Other agents cause immediate irritation with potential for more severe delayed effects. Ammonia hydrolyses to caustic ammonium hydroxide. Chlorine (pungent, greenish gas) hydrolyses to hydrochloric acid. Perfluoroisobutylene is a toxic product of Teflon. Nitrogen oxides are components of blast weapons or fire.

Treatment: Phosgene has no antidote. Good decontamination and symptomatic treatment are needed. Treatment of other agents is similar; all agents in this class are gases with no antidotes.

*others include red (RP) and white phosphorus, sulfur trioxide-chlorosulfonic acid (FS), titanium tetrachloride (FM), and zinc oxide (HZ).

51
Q

Chemical Agent (military name): Incapacitating agents

A

Examples: BZ/agent 15 (glycolate anticholinergic), cannabinoids, fentanyls and other opioids, lysergic acid diethylamide (LSD), and pheothiazines

Clinical Features: These include a variety of fast-acting CNS and respiratory depressants, often with hallucinogenic properties.

Treatment: Management is decontamination with supportive treatment; antidotes should be used when they exist (physostigmine for anticholinergics and naloxone for opioids).

52
Q

Chemical Agent (military name): Vomiting agents

A

Examples: Adamsite (DM), diphenylchloroarsine (DA), and diphenylcyanoarsine (DC)

Clinical Features: Rapidly incapacitating, irritant gases.

Treatment: Symptomatic measures are taken for sneezing, coughing, and vomiting (e.g. antiemetics).

53
Q

Chemical Agent (military name): Riot Control and Tear Gases

A

Examples: Chloroacetophenone (CN) in several solvents and chloropicrin (PS), bromobenzylcyanide (CA), dibenzoxazepine (CR), and 2-chlorobenzalmalononitrile (CS) gases

Clinical Features: Lacrimation.

Treatment: Treatment is symptomatic after decontamination. No antidotes are available.

54
Q

Acute Toxicity

A

Occurs within minutes to hours of a single exposure episode of a toxin.

Typically, unintentional poisonings in children and intentional drug overdoses in adolescents or adults (suicide attempts or drug abuse) are acute episodes).

55
Q

Chronic Toxicity

A

Typically occurs from multiple or long-term exposure to toxins. The amount may not be toxic with an acute exposure, but the chronic exposure may lead to accumulation or toxin-induced conditions that decrease elimination.

Exposures in the occupational setting, from environmental contamination, or from long-term drug abuse can lead to chronic toxicity.