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61 Cards in this Set
- Front
- Back
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List the 5 options for decontamination of a patient if she has a gastric exposure to a poison.
How efficacious are each of these methods? |
Gastric decontamination:
1) Emesis with ipecac - removes 25% of gastric contents 2) Gastric lavage - removes 30% of gastric contents 3) Whole bowel irrigation - very effective when used with charcoal 4) Activated charcoal - removes up to 90% of toxin 5) Cathartics |
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Whole bowel irrigation presents the major concern of this adverse effect:
a) aspiration b) constipation c) electrolyte loss |
Whole bowel irrigation presents the major concern of this adverse effect:
c) electrolyte loss |
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Describe the methods of decontamination for the following exposures:
1) respiratory 2) dermal 3) ocular |
1) Respiratory - get patient to fresh air and give O2 if needed
2) Dermal - remove exposed clothing and wash skin with soap and water 3) Ocular - flush with water or saline for at least 10 minutes |
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Activated charcoal absorbs most toxins except...
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Activated charcoal is not useful when the toxin is..
--a metal (Pb, Li, Fe) --a low MW alcohol -- alipliatic hydrocarbons --a caustic agent |
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Once you decontaminate your patient, what are your three management goals/options?
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Post-contamination management:
1) supportive 2) antidote 3) extracorporeal removal |
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What are the indications for extracorporeal removal of toxins?
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Extracorporeal removal is useful for:
--methanol ingestion --ethylene glycol --salicylate --theophylline --lithium |
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DON'T FORGET THE ABC'S!
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Airway
Breathing Cardiac |
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Under what circumstances are the following gastric decontamination options useful?
1) Ipecac 2) Gastric lavage 3) Activated charcoal 4) Whole bowel irrigation |
1) Ipecac - give within 1hr and patient must be conscious
2) Gastric lavage - used within 1 hr 3) Activated charcoal - absorbs most toxins except for metals, caustics, others 4) Whole bowel irrigation - useful for slowly absorbed materials and often used with charcoal |
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Match the following antidotes to their respective toxin (acetaminophen, methanol, organophosphates, metals).
1) Pralidoxime 2) Chelators 3) Ethanol 4) N-acetylcysteine |
1) Pralidoxime // organophosphates
2) Chelators // metals 3) Ethanol // methanol 4) N-acetylcysteine // acetaminophen |
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TRUE or FALSE
Normal lab values for serum lead range from 50 to 170 µg/dL. |
FALSE
The human body has no lead requirement. 50 to 170 µg/dL is actually the normal range for serum iron. |
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TRUE or FALSE
Ingested lead is absorbed rapidly from the small intestine while lead in the form of vapor is absorbed in negligible amounts. |
FALSE
True statement: Ingested lead is absorbed SLOWLY from the small intestine while lead in the form of vapor is absorbed RAPIDLY from the lungs |
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TRUE or FALSE
Lead distributes rapidly into soft tissues but is not taken up by bone. |
FALSE
True statement: Lead distributes rapidly to BOTH soft tissues and bone. |
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Compare the half-life of lead in soft tissues compared to that in the bone.
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In soft tissues, lead has a half life of 35-40 days.
In the bone, lead has a half life on the order of decades. |
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Lead poisoning may be the cause of all the of the following EXCEPT:
a) irritability b) seizures c) constipation d) rash e) reproductive issues f) anemia |
Lead poisoning does not cause a rash, but it may cause the following:
--irritability --seizures --constipation --reproductive issues --anemia --hypertiension --limb pain --metallic taste --behavioral problems --decreased IQ |
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What is the primary concern in treating a patient with lead poisoning?
a) chelation b) Fe supplements if the patient is anemic c) administering pralidoxime d) removing the patient from the lead exposure (home, job site, etc) |
What is the primary concern in treating a patient with lead poisoning?
d) removing the patient from the lead exposure (home, job site, etc) |
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What are your options for treating a patient with organophosphate poisoning?
How does this differ from treating carbamate poisoning? |
For organophosphates and carbamates, atropine is an appropriate antidote. Atropine blocks ACh receptors at the nerve endings.
Pralidoxime treats organophosphate ingestions but is usually not needed for carbamates. Pralidoxime reverses the binding of organophosphates to AChE and degrades some organophosphates. |
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TRUE or FALSE
Lead is a neurotoxin and may cause ADHD in children. |
TRUE
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All of the following are true of lead EXCEPT:
a) It is the most common preventable public health problem affecting kids in the industrialized world. b) Treatment of lead poisoning can reverse neurologic injury. c) Lead can cause decreased IQ and behavioral problems in children. d) Lead acts as a calcium substitute and plays a major role in the poor development of neural cell interactive pathways. |
These statements ARE true of lead:
a) It is the most common preventable public health problem affecting kids in the industrialized world. c) Lead can cause decreased IQ and behavioral problems in children. d) Lead acts as a calcium substitute and plays a major role in the poor development of neural cell interactive pathways. This is FALSE: b) Treatment of lead poisoning can reverse neurologic injury. Fact is, treatment does not reverse neurologic injury caused by lead poisoning. |
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What is the mechanism of action of organophosphate toxicity?
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Organophosphates and carbamates inhibit AChE.
Organophosphates are irreversible inhibitors of both AChE and pseudo-cholinesterase while carbamates reversibly inhibit these enzymes. These agents cause accumulation of ACh at nerve junctions. |
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What are the signs and symptoms of AChE inhibitor exposure?
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Life-threatening symptoms: respiratory failure, cardiac dysrhythmias, seizures.
Other symptoms: DUMBELS Diarrhea, urinary incontinence, miosis, bronchospasm, emesis, lacrimation, salivation |
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All of the following are true of organocholrine compounds EXCEPT:
a) An example of an organocholrine is DDT. b) Organocholrines are neurotoxins and interfere with axonal transmission. c) Several antidotes exist for treatment of organocholrine poisoning. d) Organocholrines bioaccumulate and are eliminated very slowly. |
These statements ARE TRUE of organocholrines:
a) An example of an organocholrine is DDT. b) Organocholrines are neurotoxins and interfere with axonal transmission. d) Organocholrines bioaccumulate and are eliminated very slowly. The FALSE statement: c) Several antidotes exist for treatment of organocholrine poisoning. In fact, there are NO antidotes for organocholrine poisoning. |
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TRUE or FALSE
While pyrethrins paralyze insects, they have little effect in humans (except for maybe causing an allergic reaction). |
TRUE
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All of the following are true of acetaminophen EXCEPT:
a) Glucuronidation metabolism of acetaminophen yields the active intermediate, NAPQI. b) Taken in therapeutic doses, it is absorbed rapidly, but taken in toxic doses, it is absorbed slowly. c) When taken as directed, the half-life of acetaminophen is 2-3hours. |
The following ARE TRUE of acetaminophen:
b) Taken in therapeutic doses, it is absorbed rapidly, but taken in toxic doses, it is absorbed slowly. c) When taken as directed, the half-life of acetaminophen is 2-3hours. FALSE statement: a) Glucuronidation metabolism of acetaminophen yields the active intermediate, NAPQI. Fact is, glucuronidation and sulfation yield non-toxic metabolites while P450 metabolism yields the active metabolite, NAPQI. |
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In acute ingestions, acetaminophen levels peak at:
a) 2 hours b) 4 hours c) 8 hours |
In acute ingestions, acetaminophen levels peak at:
b) 4 hours. |
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What happens in an acetaminophen overdose to cause hepatic necrosis?
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In an acetaminophen overdose, active metabolites are produced by P450 metabolism. Under normal circumstances, these NAPQI intermediates are detoxified by glutathione. However, in the case of an overdose, glutathione is depleted and the NAPQI intermediates bind to hepatocytes and cause hepatic necrosis.
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Briefly describe the 4 phases of acetaminophen toxicity.
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PHASE 1 (0-24h)
Patient may be either asymptomatic or may have GI symptoms. PHASE 2 (24-72h) Chemical vidence of hepatic dysfunction develops. PHASE 3 (72-96h) Frank liver failure. PHASE 4 Patient will either recover without many complications, will die or will need a transplant. |
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How do you diagnose acetaminophen toxicity?
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Acetaminophen levels should be drawn at 4 hours post-ingestion.
In the case of acute ingestions, a nomogram should be used to determine if the patient needs treatment. In the case of chronic ingestion, a nomogram cannot be used. Instead, APAP levels, LFT's and the presence of GI symptoms should be used to determine whether or not you should treat the patient. |
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What is the antidote for acetaminophen?
What are the guidelines for its use? |
N-acetylcysteine (NAC) is the antidote for acetaminophen overdose.
It should be given within 8h of ingestion but may be of benefit up to 24h post-ingestion. It is given IV as a 1 day course. |
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Describe the mechanism of action of simple asphyxiants such as helium and methane.
If your patient has been exposed to, say, helium gas, how will he present? |
Simple asphyxiants displace oxygen from the environment and exposure often occurs in confined spaces or in concentrated forms. These gases do not have inherent toxicity.
Signs and symptoms are related to hypoxemia. |
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Describe the mechanism of action of chemical asphyxiants like CO, cyanide, and hydrogen sulfide.
If your patient has been exposed to, say, carbon monoxide due to malfunctioning heating equipment, how will he present? |
Chemical asphyxiants bind to hemoglobin (carbon monoxide) and cytochrome oxidase (cyanide). They may also bind to various enzymes which would manifest clinically.
Signs and symptoms are related to hypoxemia. Major affected systems involved are the heart and CNS. |
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Your patient has carbon monoxide poisoning.
How do you treat him? |
Treatment in ALL cases centers on removal of the patient from the carbon monoxide source, giving supplemental oxygen and supportive care.
High flow oxygen, and maybe even hyperbaric oxygen, may be given in the case of CO toxicity. |
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Your patient works as a chemist and has cyanide poisoning.
How do you treat him? |
Treatment in ALL cases centers on removal of the patient from the carbon monoxide source, giving supplemental oxygen and supportive care.
Hydroxocobalamin is a cyanide antidote. It is converted to cyanocobalamin in the body, which is vitamin B12. |
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Which of the following toxic gases produce injury to the mucosal lining of the respiratory tract?
a) carbon monoxide b) cyanide c) helium d) ammonia |
Which of the following produce injury to the mucosal lining of the respiratory tract?
Answer: d) ammonia Other answer choices: a) carbon monoxide - binds hemoglobin b) cyanide - binds cytochrome oxidase c) helium - simple asphyxiant |
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These highly water soluble gases interact with the upper respiratory tract to cause oral and nasal pain and a cough.
a) ammonia, chloramine, hydrogen chloride b) carbon monoxide, cyanide c) phosgene, chlorine |
These highly water soluble gases interact with the upper respiratory tract to cause oral and nasal pain and a cough.
a) ammonia, chloramine, hydrogen chloride |
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What are the key differences between the various irritant gases in regards to the onset of clinical symptoms and site of injury?
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Irritant gases come in 3 flavors: high water solubility, intermediate water solubility, and low water solubility.
High water solubility: produce rapid onset of clinical effects and primarily cause upper tract injury. (ammonia, chloramine, HCl) Intermediate cause some delay in onset of symptoms and cause injury to both lower and upper tracts. (chlorine) Low solubility gases produce very delayed effects (many hours) and primarily injure the lower tract. (phosgene) |
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For the following gases, identify its classification (simple, irritant, etc) and its mechanism of action.
1) carbon monoxide 2) helium and methane 3) ammonia 4) phosgene 5) hydrogen chloride and chloramine 6) cyanide 7) chlorine |
1) carbon monoxide = chemical asphyxiant that binds to hemoglobin
2) helium and methane = simple asphyxiants that displace oxygen from the environment 3) ammonia = highly water soluble irritant gas that primarily injures the upper respiratory tract 4) phosgene = low water solubility irritant gas that primarily injures the lower respiratory tract 5) hydrogen chloride and chloramine = highly water soluble irritant gase that primarily injures the upper respiratory tract 6) cyanide = chemical asphyxiant that binds to cytochrome oxidase 7) chlorine = intermediate water solublility irritant gase that injures both the lower and upper respiratory tracts |
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Treatment of toxic gas exposure centers on:
a) removal from source, antidote, and activated charcoal b) removal from source, removal of clothing, and washing with soap and water c) removal from source, supplemental oxygen, supportive care |
Treatment of toxic gas exposure centers on:
c) removal from source, supplemental oxygen, supportive care |
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What symptoms might you expect in a child who ingested kerosene?
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Immediate pulmonary symptoms: coughing, gasping, choking, chest pain, cyanosis
Systemic symptoms: headache, sedation, confusion, seizures, coma, cardiac dysrhythmias, nausea, vomiting |
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A young child is brought to the Kosair ER. He is coughing, gasping and sputtering. His mom tells you that she caught him drinking kerosene.
What should your initial evaluation include? |
Initially, you need to evaluate the patient's symptoms to determine if he is asymptomatic, or has mild (occasional cough, N/V) or major (progressive respiratory) symptoms.
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Hydrocarbon toxicity is related to:
a) viscosity b) volatility c) surface tension d) all of the above |
Hydrocarbon toxicity is related to:
d) all of the above (viscosity, volatility, surface tension) |
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TRUE or FALSE
Hydrocarbons (gasoline, lighter fluid) with the highest viscosity produce the most lung injury. |
FALSE
True statement: Hydrocarbons (gasoline, lighter fluid) with the LOWEST viscosity produce the most lung injury. |
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What is the pathophysiology behind hydrocarbon toxicity?
(think about properties of the hydrocarbons, their effects on certain organs, etc) |
Hydrocarbons have low surface tension and low viscosity. When they are either inhaled or aspirated, these physical properties allow a small amount to spread over a large pulmonary surface. The hydrocarbons destroy surfactant, and can cause chemical pneumonitis which may progress to ARDS.
Hydrocarbons can also cause systemic toxicity including: GI irritation, renal damage, and eye and skin irritation. If aspirated, CNS depression and coma can result due to hypoxia. |
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TRUE or FALSE
Signs and symptoms of hydrocarbon ingestion depend not only on the route of hydrocarbon exposure, its chemical structure, physical properties, and the amount ingested - but also on the age of the patient who ingests it. |
TRUE
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TRUE or FALSE
Steroids and antibiotics are effective in the treatment of pneumonia secondary to hydrocarbon ingestion. |
FALSE
True statement: Antibiotics are not given prophylactically and steroids are of no proven value in this scenario. |
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A mother finds her 4yr old daughter with a container of gasoline in the garage. The child is rushed to the ER where her mom tells you that her daughter was coughing and sputtering when she found her. The child is now wheezing and tachypneic. She is visibly cyanotic. Her clothes are stained with gasoline.
What is your treatment approach? |
1) Remove contaminated clothing ans wash exposed skin with soap and water.
2) Kerosene is a simple hydrocarbon and does not need to be removed from the stomach, so do not induce emesis! 3) Get a chest XRay. 4) The child has major symptoms as her initial respiratory symptoms (coughing and sputtering) have gotten progressively worse. She should be hospitalized. 4) Get another chest XRay in 6-12hours. 5) If the child has clinical evidence of pneumonitis, treat her! |
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TRUE or FALSE
When considering treating a patient who ingested hydrocarbon, it is important to remember to treat the patient and not the chest xray since 1/3 of asymptomatic patients may have abnormal CXR findings. |
TRUE
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Describe therapy for hydrocarbon-induced ARDS or severe pneumonitis?
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1) Mechanical ventilation (oxygen/PEEP)
2) Extracorporeal Life Support |
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Describe "sudden sniffing death syndrome".
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Sudden sniffing death syndrome results from hydrocarbon induced myocardial sensitivity to epinephrine and a sudden surge of epinephrine 2ndary to the startle reflex with a resultant fatal cardiac dysrhythmia.
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All of the following are true of inhalation abuse and inhalants EXCEPT:
1) Most common cause of death is by asphyxiation. 2) Peak age of inhalation abuse is 13-15 years. 3) Inhalation abuse is the intentional inhalation of a volatile substance for the purpose of achieving a euphoric state. 4) Inhalants are depressants. |
These ARE TRUE statements:
2) Peak age of inhalation abuse is 13-15 years. 3) Inhalation abuse is the intentional inhalation of a volatile substance for the purpose of achieving a euphoric state. 4) Inhalants are depressants. The FALSE statement: 1) Most common cause of death is by asphyxiation. Fact is, the most common cause of death is due to the "sudden sniffing death syndrome". Death caused by asphyxiation is negligible. |
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All of the following are true of inhalation abuse and inhalants EXCEPT:
1) Inhaling a volatile substance can cause euphoria, slurred speech, chest pain and asphyxia. 2) Inhalation abuse can lead to loss of brain mass and deafness. 3) Respiratory arrest can result from laryngospasms that are induced by inhaling cold aerosols. 4) People who inhale volatile substances often fall into a coma within 10 minutes. |
These ARE TRUE statements:
1) Inhaling a volatile substance can cause euphoria, slurred speech, chest pain and asphyxia. 2) Inhalation abuse can lead to loss of brain mass and deafness. 3) Respiratory arrest can result from laryngospasms that are induced by inhaling cold aerosols. The FALSE statement: 4) People who inhale volatile substances often fall into a coma within 10 minutes. Fact is, when a person inhales a volatile substance, he/she will experience euphoria, followed by drowsiness and sleep. Progression to coma is unusual since the user often terminates inhalant use when he/she becomes drowsy. |
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What are some clinical CNS signs and symptoms of inhalation abuse?
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CNS signs/symptoms of inhalant use:
--hallucinations --appearing intoxicated --euphoria --clouding of consciousness --seizures --tinnitus --slurred speech --sedation --headache |
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What are the clinical signs and symptoms (other than those relating to the CNS) of inhalation abuse?
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Systemic signs/symptoms of inhalation use:
--blurred vision --perioral pyodermas --chest pain --bronchospasm --abdominal pain |
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How do you treat a patient with inhalation abuse? (short term and long term)
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In the short-term, decontaminate the patient and use symptomatic treatment as necessary (oxygen, anticonvulsants, antiarrhythmics).
In the long-term, counseling and educating the patient is a must. |
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Describe the pathophysiology of iron toxicity.
Which organ systems are primarily affected? |
Initially, iron toxicity causes corosive mucosal damage to the stomach and small intestine. Hydrogen ions are produced, leading to the generation of vasoactive substances, venous pooling and eventual shock. Hemorrhagic necrosis and perforation may also occur.
Unbound serum iron uncouples oxidative phosphorylation and results in radical formation. Primary organ systems affected: GI, hemodynamic, metabolic/electrolytes, CNS |
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Name the antidote used for iron poisoning.
What is its mechanism of action? What are the indications for its use? |
Deferoxamine chelates iron by pulling it out of the mitochondria and cells by mass action to form water-soluble ferrioxamine (which is renally excreted).
Indications for its use is when serum iron is >500 mcg/dl or when significant signs and symptoms are evident below this level. |
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All of the following are true of the treatment of iron poisoning EXCEPT:
1) In most clinical settings, when serum iron levels fall below the range of 100-150 mcg/dl, deferoxamine is discontinued. 2) Serum iron level of 350 mcg/dl + significant systemic symptoms of iron overload is indication for deferoxamine chelation. 3) Complexation therapy using bicarbonate is usually not recommended. 4) Charcoal decontamination is extremely effective in treating iron toxicity. |
These ARE TRUE statements:
1) In most clinical settings, when serum iron levels fall below the range of 100-150 mcg/dl, deferoxamine is discontinued. 2) Serum iron level of 350 mcg/dl + significant systemic symptoms of iron overload is indication for deferoxamine chelation. 3) Complexation therapy using bicarbonate is usually not recommended. The FALSE statement: 4) Charcoal decontamination is extremely effective in treating iron toxicity. In fact, charcoal decontamination is NOT effective in adsorbing iron. |
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All of the following are true of iron and iron poisoning EXCEPT:
1) Iron levels do not correlate with the 4 phases of iron toxicity. 2) TIBC levels can better predict the severity of iron poisoning compared to erum iron levels. 3) If a patient suspected of taking an iron overdose does not develop symptoms after 6 hours, it is unlikely that she will become symptomatic. 4) A lethal dose of elemental iron is between 180-300 mg/kg. |
These ARE TRUE statements:
1) Iron levels do not correlate with the 4 phases of iron toxicity. 3) If a patient suspected of taking an iron overdose does not develop symptoms after 6 hours, it is unlikely that she will become symptomatic. 4) A lethal dose of elemental iron is between 180-300 mg/kg. The FALSE statement: 2) TIBC levels can better predict the severity of iron poisoning compared to erum iron levels. Fact is, TIBC is not readily available measurement is not reliable when evaluating a person with suspected iron poisoning. Serum iron levels obtained 4-6hrs after ingestion, however, can predict the severity of poisoning. |
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Describe the symptoms seen during the 4 clinical phases of iron toxicity.
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PHASE I (0-6hrs)
N/V, hematemesis, pallor, hemorrhagic diarrhea, abdominal pain, tachycardia, hypotension, leukocytosis, acidosis PHASE II (6-24hrs) temporary recover PHASE III (8-48hrs) GI, obtundation, coma, pulmonary edema, shock, seizures, clotting abnormalities PHASE IV (2days - 3weeks) ARDS, cirrhosis, sepsis, pyloric stenosis |
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All of the following are late findings (1 week post-ingestion) of iron toxicity EXCEPT:
a) pyloric stenosis b) ARDS c) hemorrhagic diarrhea d) sepsis e) cirrhosis |
All of the following are late findings (1 week post-ingestion) of iron toxicity EXCEPT:
c) hemorrhagic diarrhea |
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TRUE or FALSE
A patient who ingests gasoline and is immediately symptomatic is at a higher risk for developing aspiration penumonia/ARDS compared to a person who doesn't develop symptoms until later. |
TRUE
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Sodium bicarbonate treatment may improve symptoms in:
a) acid inhalations b) acid ingestions c) both d) neither |
Nebulized sodium bicarbonate may improve symptoms in:
a) acid inhalations Nebulized sodium bicarbonate may improve symptoms in acid inhalations (hydrogen chloride) and inhaalations which resutl in acid formation (chloramine). |
